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Tytuł:
Microenvironment-induced downregulation of miR-193b drives ovarian cancer metastasis.
Autorzy:
Mitra AK; Department of Obstetrics and Gynecology, Section of Gynecologic Oncology - Center for Integrative Science, University of Chicago, Chicago, IL, USA.; Medical Sciences Program, Indiana University School of Medicine, Indiana University, Bloomington, IN, USA.
Chiang CY; Department of Obstetrics and Gynecology, Section of Gynecologic Oncology - Center for Integrative Science, University of Chicago, Chicago, IL, USA.
Tiwari P; Department of Obstetrics and Gynecology, Section of Gynecologic Oncology - Center for Integrative Science, University of Chicago, Chicago, IL, USA.
Tomar S; Medical Sciences Program, Indiana University School of Medicine, Indiana University, Bloomington, IN, USA.
Watters KM; Department of Obstetrics and Gynecology, Section of Gynecologic Oncology - Center for Integrative Science, University of Chicago, Chicago, IL, USA.
Peter ME; Division of Hematology/Oncology, Northwestern University, Feinberg School of Medicine, Chicago, IL, USA.
Lengyel E; Department of Obstetrics and Gynecology, Section of Gynecologic Oncology - Center for Integrative Science, University of Chicago, Chicago, IL, USA.
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Źródło:
Oncogene [Oncogene] 2015 Nov 26; Vol. 34 (48), pp. 5923-32. Date of Electronic Publication: 2015 Mar 23.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
MeSH Terms:
Cell Movement*
Gene Expression Regulation, Neoplastic*
Tumor Microenvironment*
MicroRNAs/*genetics
Omentum/*pathology
Ovarian Neoplasms/*genetics
Ovarian Neoplasms/*pathology
Animals ; Apoptosis ; Blotting, Western ; Cell Adhesion ; Cell Proliferation ; Female ; Humans ; Immunoenzyme Techniques ; Mice ; Mice, Nude ; Omentum/metabolism ; Ovarian Neoplasms/metabolism ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Cells, Cultured ; Urokinase-Type Plasminogen Activator/genetics ; Urokinase-Type Plasminogen Activator/metabolism ; Xenograft Model Antitumor Assays
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
DNA methylation in small cell lung cancer defines distinct disease subtypes and correlates with high expression of EZH2.
Autorzy:
Poirier JT; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Gardner EE; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.; Department of Pharmacology and Molecular Sciences, Johns Hopkins University, Baltimore, MD, USA.
Connis N; Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Moreira AL; Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
de Stanchina E; Molecular Pharmacology & Chemistry Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Hann CL; Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Rudin CM; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.; Department of Pharmacology and Molecular Sciences, Johns Hopkins University, Baltimore, MD, USA.
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Źródło:
Oncogene [Oncogene] 2015 Nov 26; Vol. 34 (48), pp. 5869-78. Date of Electronic Publication: 2015 Mar 09.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural
MeSH Terms:
DNA Methylation*
Gene Expression Regulation, Neoplastic*
Biomarkers, Tumor/*analysis
Lung Neoplasms/*classification
Polycomb Repressive Complex 2/*genetics
Polycomb Repressive Complex 2/*metabolism
Small Cell Lung Carcinoma/*classification
Animals ; Blotting, Western ; CpG Islands ; Enhancer of Zeste Homolog 2 Protein ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Mice ; Polycomb Repressive Complex 2/antagonists & inhibitors ; Promoter Regions, Genetic ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Small Cell Lung Carcinoma/genetics ; Small Cell Lung Carcinoma/metabolism ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
Tumor-specific signaling to p53 is mimicked by Mdm2 inactivation in zebrafish: insights from mdm2 and mdm4 mutant zebrafish.
Autorzy:
Chua JS; p53 Laboratory, Biomedical Sciences Institutes, Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
Liew HP; p53 Laboratory, Biomedical Sciences Institutes, Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
Guo L; Aegis Biotech, Singapore, Singapore.
Lane DP; p53 Laboratory, Biomedical Sciences Institutes, Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
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Źródło:
Oncogene [Oncogene] 2015 Nov 26; Vol. 34 (48), pp. 5933-41. Date of Electronic Publication: 2015 Mar 09.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:
Animals, Genetically Modified/*metabolism
Eye Neoplasms/*pathology
Mutation/*genetics
Proto-Oncogene Proteins c-mdm2/*metabolism
Tumor Suppressor Protein p53/*metabolism
Zebrafish/*metabolism
Zebrafish Proteins/*metabolism
Animals ; Animals, Genetically Modified/embryology ; Animals, Genetically Modified/genetics ; Blotting, Western ; Embryo, Nonmammalian/metabolism ; Embryo, Nonmammalian/pathology ; Eye Neoplasms/genetics ; Eye Neoplasms/metabolism ; Gene Expression Regulation, Developmental ; Mice ; Phenotype ; Proto-Oncogene Proteins c-mdm2/genetics ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Tumor Suppressor Protein p53/genetics ; Zebrafish/embryology ; Zebrafish/genetics ; Zebrafish Proteins/genetics
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
PPM1D phosphatase, a target of p53 and RBM38 RNA-binding protein, inhibits p53 mRNA translation via dephosphorylation of RBM38.
Autorzy:
Zhang M; Comparative Oncology Laboratory, Department of Surgical & Radiological Sciences, School of Veterinary Medicine, University of California, Davis, Davis, CA, USA.
Xu E; Comparative Oncology Laboratory, Department of Surgical & Radiological Sciences, School of Veterinary Medicine, University of California, Davis, Davis, CA, USA.
Zhang J; Comparative Oncology Laboratory, Department of Surgical & Radiological Sciences, School of Veterinary Medicine, University of California, Davis, Davis, CA, USA.
Chen X; Comparative Oncology Laboratory, Department of Surgical & Radiological Sciences, School of Veterinary Medicine, University of California, Davis, Davis, CA, USA.
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Źródło:
Oncogene [Oncogene] 2015 Nov 26; Vol. 34 (48), pp. 5900-11. Date of Electronic Publication: 2015 Mar 30.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural
MeSH Terms:
Gene Expression Regulation, Neoplastic*
Breast Neoplasms/*metabolism
Colonic Neoplasms/*metabolism
Phosphoprotein Phosphatases/*metabolism
RNA, Messenger/*metabolism
RNA-Binding Proteins/*metabolism
Tumor Suppressor Protein p53/*metabolism
3' Untranslated Regions/genetics ; Blotting, Western ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Colonic Neoplasms/genetics ; Colonic Neoplasms/pathology ; Female ; Flow Cytometry ; Humans ; Immunoenzyme Techniques ; Immunoprecipitation ; Phosphoprotein Phosphatases/antagonists & inhibitors ; Phosphoprotein Phosphatases/genetics ; Phosphorylation ; Protein Phosphatase 2C ; RNA Processing, Post-Transcriptional ; RNA, Messenger/genetics ; RNA, Small Interfering/genetics ; RNA-Binding Proteins/antagonists & inhibitors ; RNA-Binding Proteins/genetics ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/antagonists & inhibitors ; Tumor Suppressor Protein p53/genetics
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
CCAAT/Enhancer binding protein β controls androgen-deprivation-induced senescence in prostate cancer cells.
Autorzy:
Barakat DJ; Division of Pediatric Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Zhang J; Division of Pediatric Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Barberi T; Division of Pediatric Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Denmeade SR; Division of Medical Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Friedman AD; Division of Pediatric Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
Paz-Priel I; Division of Pediatric Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA.
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Źródło:
Oncogene [Oncogene] 2015 Nov 26; Vol. 34 (48), pp. 5912-22. Date of Electronic Publication: 2015 Mar 16.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
MeSH Terms:
Androgens/*deficiency
Androgens/*pharmacology
CCAAT-Enhancer-Binding Protein-beta/*metabolism
Cellular Senescence/*drug effects
Gene Expression Regulation, Neoplastic/*drug effects
Prostatic Neoplasms/*pathology
Apoptosis/drug effects ; Blotting, Western ; CCAAT-Enhancer-Binding Protein-beta/genetics ; Cell Proliferation/drug effects ; Chromatin Immunoprecipitation ; Flow Cytometry ; Fluorescent Antibody Technique ; Humans ; Immunoenzyme Techniques ; Male ; Promoter Regions, Genetic/genetics ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/metabolism ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Transcription, Genetic/drug effects ; Tumor Cells, Cultured
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
Cell growth density modulates cancer cell vascular invasion via Hippo pathway activity and CXCR2 signaling.
Autorzy:
Sharif GM; Lombardi Cancer Center, Georgetown University, Washington, DC, USA.
Schmidt MO; Lombardi Cancer Center, Georgetown University, Washington, DC, USA.
Yi C; Lombardi Cancer Center, Georgetown University, Washington, DC, USA.
Hu Z; Lombardi Cancer Center, Georgetown University, Washington, DC, USA.
Haddad BR; Lombardi Cancer Center, Georgetown University, Washington, DC, USA.
Glasgow E; Lombardi Cancer Center, Georgetown University, Washington, DC, USA.
Riegel AT; Lombardi Cancer Center, Georgetown University, Washington, DC, USA.
Wellstein A; Lombardi Cancer Center, Georgetown University, Washington, DC, USA.
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Źródło:
Oncogene [Oncogene] 2015 Nov 26; Vol. 34 (48), pp. 5879-89. Date of Electronic Publication: 2015 Mar 16.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural
MeSH Terms:
Cell Movement*
Gene Expression Regulation, Neoplastic*
Adaptor Proteins, Signal Transducing/*metabolism
Breast Neoplasms/*metabolism
Breast Neoplasms/*pathology
Endothelium, Vascular/*pathology
Phosphoproteins/*metabolism
Protein Serine-Threonine Kinases/*metabolism
Receptors, Interleukin-8B/*metabolism
Adaptor Proteins, Signal Transducing/genetics ; Animals ; Apoptosis ; Blotting, Western ; Breast Neoplasms/genetics ; Cell Cycle ; Cell Proliferation ; Cytokines/genetics ; Cytokines/metabolism ; Endothelium, Vascular/metabolism ; Female ; Human Umbilical Vein Endothelial Cells ; Humans ; Mice ; Mice, Nude ; Neoplasm Invasiveness ; Phosphoproteins/genetics ; Phosphorylation ; Protein Serine-Threonine Kinases/antagonists & inhibitors ; Protein Serine-Threonine Kinases/genetics ; RNA Interference ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Receptors, Interleukin-8B/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Transcription Factors ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays ; YAP-Signaling Proteins ; Zebrafish
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
TM9SF4 is a novel V-ATPase-interacting protein that modulates tumor pH alterations associated with drug resistance and invasiveness of colon cancer cells.
Autorzy:
Lozupone F; Therapeutic Research and Medicines Evaluation Department, Istituto Superiore di Sanità, Rome, Italy.
Borghi M; Infectious, Parasitic and Immune-Mediated Diseases Department, Istituto Superiore di Sanità, Rome, Italy.
Marzoli F; Therapeutic Research and Medicines Evaluation Department, Istituto Superiore di Sanità, Rome, Italy.
Azzarito T; Therapeutic Research and Medicines Evaluation Department, Istituto Superiore di Sanità, Rome, Italy.
Matarrese P; Therapeutic Research and Medicines Evaluation Department, Istituto Superiore di Sanità, Rome, Italy.
Iessi E; Therapeutic Research and Medicines Evaluation Department, Istituto Superiore di Sanità, Rome, Italy.
Venturi G; Therapeutic Research and Medicines Evaluation Department, Istituto Superiore di Sanità, Rome, Italy.
Meschini S; Technology and Health Department, Istituto Superiore di Sanità, Rome, Italy.
Canitano A; Therapeutic Research and Medicines Evaluation Department, Istituto Superiore di Sanità, Rome, Italy.
Bona R; Therapeutic Research and Medicines Evaluation Department, Istituto Superiore di Sanità, Rome, Italy.
Cara A; Therapeutic Research and Medicines Evaluation Department, Istituto Superiore di Sanità, Rome, Italy.
Fais S; Therapeutic Research and Medicines Evaluation Department, Istituto Superiore di Sanità, Rome, Italy.
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Źródło:
Oncogene [Oncogene] 2015 Oct 01; Vol. 34 (40), pp. 5163-74. Date of Electronic Publication: 2015 Feb 09.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:
Colonic Neoplasms/*pathology
Drug Resistance, Neoplasm/*physiology
Membrane Proteins/*metabolism
Neoplasm Invasiveness/*pathology
Vacuolar Proton-Translocating ATPases/*metabolism
Blotting, Western ; Cell Line, Tumor ; Colonic Neoplasms/metabolism ; Fluorescence Resonance Energy Transfer ; Humans ; Hydrogen-Ion Concentration ; Immunoprecipitation ; Microscopy, Confocal ; Polymerase Chain Reaction ; Transfection
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
A novel recurrent CHEK2 Y390C mutation identified in high-risk Chinese breast cancer patients impairs its activity and is associated with increased breast cancer risk.
Autorzy:
Wang N; Department of Oncology, Changhai Hospital, the Second Military Medical University, Shanghai, China.
Ding H; Key Laboratory of Systems Biology, State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Liu C; Department of Oncology, Changhai Hospital, the Second Military Medical University, Shanghai, China.; Key Laboratory of Systems Biology, State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Li X; Key Laboratory of Systems Biology, State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Wei L; Department of Oncology, Changhai Hospital, the Second Military Medical University, Shanghai, China.; Department of Oncology, the 401 hospital of PLA, Qingdao, China.
Yu J; Key Laboratory of Systems Biology, State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Liu M; Key Laboratory of Systems Biology, State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Ying M; Department of Oncology, Changhai Hospital, the Second Military Medical University, Shanghai, China.
Gao W; Department of Oncology, Changhai Hospital, the Second Military Medical University, Shanghai, China.
Jiang H; Key Laboratory of Systems Biology, State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Wang Y; Department of Oncology, Changhai Hospital, the Second Military Medical University, Shanghai, China.; Xinhua Cancer Center, Xinhua Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
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Źródło:
Oncogene [Oncogene] 2015 Oct 01; Vol. 34 (40), pp. 5198-205. Date of Electronic Publication: 2015 Jan 26.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:
Germ-Line Mutation*
Asian People/*genetics
Checkpoint Kinase 2/*genetics
Genetic Predisposition to Disease/*genetics
Adult ; Blotting, Western ; Breast Neoplasms/genetics ; DNA Mutational Analysis ; Female ; Humans ; Polymerase Chain Reaction ; Risk Factors
SCR Disease Name:
Breast Cancer, Familial
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
p73 engages A2B receptor signalling to prime cancer cells to chemotherapy-induced death.
Autorzy:
Long JS; Cancer Research UK Beatson Institute, Glasgow, UK.
Schoonen PM; Cancer Research UK Beatson Institute, Glasgow, UK.; Department of Medical Oncology, University Medical Center Groningen, Groningen, The Netherlands.
Graczyk D; Cancer Research UK Beatson Institute, Glasgow, UK.
O'Prey J; Cancer Research UK Beatson Institute, Glasgow, UK.
Ryan KM; Cancer Research UK Beatson Institute, Glasgow, UK.
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Źródło:
Oncogene [Oncogene] 2015 Oct 01; Vol. 34 (40), pp. 5152-62. Date of Electronic Publication: 2015 Feb 09.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:
Apoptosis/*physiology
DNA-Binding Proteins/*metabolism
Nuclear Proteins/*metabolism
Receptor, Adenosine A2B/*metabolism
Tumor Suppressor Proteins/*metabolism
Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Blotting, Western ; Cell Line, Tumor ; Chromatin Immunoprecipitation ; Flow Cytometry ; Gene Expression Regulation/physiology ; Gene Knockdown Techniques ; Humans ; Polymerase Chain Reaction ; RNA, Small Interfering ; Transfection ; Tumor Protein p73
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
Nuclear accumulation of annexin A2 contributes to chromosomal instability by coilin-mediated centromere damage.
Autorzy:
Kazami T; Department of Molecular Diagnosis (F8), Graduate School of Medicine, Chiba University, Inohana, Chuo-ku, Chiba, Japan.
Nie H; Department of Molecular Diagnosis (F8), Graduate School of Medicine, Chiba University, Inohana, Chuo-ku, Chiba, Japan.
Satoh M; Department of Molecular Diagnosis (F8), Graduate School of Medicine, Chiba University, Inohana, Chuo-ku, Chiba, Japan.
Kuga T; Laboratory of Proteome Research, National Institute of Biomedical Innovation, Saito-Asagi, Ibaraki City, Osaka, Japan.
Matsushita K; Department of Molecular Diagnosis (F8), Graduate School of Medicine, Chiba University, Inohana, Chuo-ku, Chiba, Japan.
Kawasaki N; 1] Department of Molecular Diagnosis (F8), Graduate School of Medicine, Chiba University, Inohana, Chuo-ku, Chiba, Japan [2] Laboratory of Proteome Research, National Institute of Biomedical Innovation, Saito-Asagi, Ibaraki City, Osaka, Japan.
Tomonaga T; 1] Department of Molecular Diagnosis (F8), Graduate School of Medicine, Chiba University, Inohana, Chuo-ku, Chiba, Japan [2] Laboratory of Proteome Research, National Institute of Biomedical Innovation, Saito-Asagi, Ibaraki City, Osaka, Japan.
Nomura F; Department of Molecular Diagnosis (F8), Graduate School of Medicine, Chiba University, Inohana, Chuo-ku, Chiba, Japan.
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Źródło:
Oncogene [Oncogene] 2015 Aug 06; Vol. 34 (32), pp. 4177-89. Date of Electronic Publication: 2014 Oct 27.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:
Chromosomal Instability*
Annexin A2/*genetics
Centromere/*genetics
Nuclear Proteins/*genetics
Aneuploidy ; Annexin A2/metabolism ; Apoptosis/genetics ; Autoantigens/genetics ; Autoantigens/metabolism ; Blotting, Western ; Caco-2 Cells ; Cell Line, Tumor ; Cell Nucleus/genetics ; Cell Nucleus/metabolism ; Centromere/metabolism ; Centromere Protein A ; Chromosomal Proteins, Non-Histone/genetics ; Chromosomal Proteins, Non-Histone/metabolism ; Electrophoresis, Gel, Two-Dimensional ; Gene Expression Regulation, Neoplastic ; HCT116 Cells ; HT29 Cells ; Humans ; Microsatellite Instability ; Nuclear Proteins/metabolism ; Proteome/genetics ; Proteome/metabolism ; Proteomics/methods ; RNA Interference ; Reverse Transcriptase Polymerase Chain Reaction
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
TET1 is a tumour suppressor that inhibits colon cancer growth by derepressing inhibitors of the WNT pathway.
Autorzy:
Neri F; Epigenetics, Human Genetics Foundation (HuGeF), Torino, Italy.
Dettori D; Epigenetics, Human Genetics Foundation (HuGeF), Torino, Italy.
Incarnato D; 1] Epigenetics, Human Genetics Foundation (HuGeF), Torino, Italy [2] Dipartimento di Biotecnologie Chimica e Farmacia, Università di Siena, Siena, Italy.
Krepelova A; 1] Epigenetics, Human Genetics Foundation (HuGeF), Torino, Italy [2] Dipartimento di Biotecnologie Chimica e Farmacia, Università di Siena, Siena, Italy.
Rapelli S; 1] Epigenetics, Human Genetics Foundation (HuGeF), Torino, Italy [2] Dipartimento di Biotecnologie Chimica e Farmacia, Università di Siena, Siena, Italy.
Maldotti M; Epigenetics, Human Genetics Foundation (HuGeF), Torino, Italy.
Parlato C; Epigenetics, Human Genetics Foundation (HuGeF), Torino, Italy.
Paliogiannis P; Dipartimento di Scienze Chirurgiche, Microchirurgiche e Mediche, Università di Sassari, Sassari, Italy.
Oliviero S; 1] Epigenetics, Human Genetics Foundation (HuGeF), Torino, Italy [2] Dipartimento di Scienze della Vita e Biologia dei Sistemi, Università di Torino Torino, Italy.
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Źródło:
Oncogene [Oncogene] 2015 Aug 06; Vol. 34 (32), pp. 4168-76. Date of Electronic Publication: 2014 Nov 03.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:
Colonic Neoplasms/*genetics
DNA-Binding Proteins/*genetics
Proto-Oncogene Proteins/*genetics
Tumor Suppressor Proteins/*genetics
Wnt Signaling Pathway/*genetics
Animals ; Antibiotics, Antineoplastic/pharmacology ; Blotting, Western ; Caco-2 Cells ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Proliferation/genetics ; Colonic Neoplasms/drug therapy ; Colonic Neoplasms/metabolism ; DNA Methylation/drug effects ; DNA Methylation/genetics ; DNA-Binding Proteins/metabolism ; Doxorubicin/pharmacology ; Flow Cytometry ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Nude ; Mixed Function Oxygenases ; Proto-Oncogene Proteins/metabolism ; RNA Interference ; Reverse Transcriptase Polymerase Chain Reaction ; Time Factors ; Tumor Burden/drug effects ; Tumor Burden/genetics ; Tumor Suppressor Proteins/metabolism ; Wnt Signaling Pathway/drug effects ; Xenograft Model Antitumor Assays
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
Manganese superoxide dismutase deficiency triggers mitochondrial uncoupling and the Warburg effect.
Autorzy:
Xu Y; Department of Oncology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Miriyala S; Graduate Center for Toxicology, University of Kentucky, Lexington, KY, USA.
Fang F; Department of Radiation Medicine, University of Kentucky, Lexington, KY, USA.
Bakthavatchalu V; Graduate Center for Toxicology, University of Kentucky, Lexington, KY, USA.
Noel T; Graduate Center for Toxicology, University of Kentucky, Lexington, KY, USA.
Schnell DM; Graduate Center for Toxicology, University of Kentucky, Lexington, KY, USA.
Wang C; Markey Cancer Center, University of Kentucky, Lexington, KY, USA.
St Clair WH; Department of Radiation Medicine, University of Kentucky, Lexington, KY, USA.
St Clair DK; 1] Graduate Center for Toxicology, University of Kentucky, Lexington, KY, USA [2] Markey Cancer Center, University of Kentucky, Lexington, KY, USA.
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Źródło:
Oncogene [Oncogene] 2015 Aug 06; Vol. 34 (32), pp. 4229-37. Date of Electronic Publication: 2014 Nov 03.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
MeSH Terms:
Glycolysis*
Mitochondria/*metabolism
Mitochondrial Proteins/*metabolism
Superoxide Dismutase/*deficiency
Adenosine Triphosphate/metabolism ; Animals ; Blotting, Western ; Cells, Cultured ; Humans ; Ion Channels/genetics ; Ion Channels/metabolism ; Lactates/metabolism ; Mice, Knockout ; Mitochondria/genetics ; Mitochondrial Proteins/genetics ; PPAR alpha/genetics ; PPAR alpha/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; RNA Interference ; Reactive Oxygen Species/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/genetics ; Superoxide Dismutase/genetics ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism ; Uncoupling Protein 1 ; Uncoupling Protein 2
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
Iterative tyrosine phosphorylation controls non-canonical domain utilization in Crk.
Autorzy:
Sriram G; Department of Biochemistry and Molecular Biology, Rutgers Biomedical and Health Sciences, Newark, NJ, USA.
Jankowski W; Department of Chemistry and Chemical Biology, Rutgers University, Piscataway, NJ, USA.
Kasikara C; Department of Biochemistry and Molecular Biology, Rutgers Biomedical and Health Sciences, Newark, NJ, USA.
Reichman C; Department of Biochemistry and Molecular Biology, Rutgers Biomedical and Health Sciences, Newark, NJ, USA.
Saleh T; Department of Chemistry and Chemical Biology, Rutgers University, Piscataway, NJ, USA.
Nguyen KQ; Department of Biochemistry and Molecular Biology, Rutgers Biomedical and Health Sciences, Newark, NJ, USA.
Li J; Cell Signaling Technology, Danvers, MA, USA.
Hornbeck P; Cell Signaling Technology, Danvers, MA, USA.
Machida K; Raymond and Beverly Sackler Laboratory of Genetics and Molecular Medicine, Department of Genetics and Developmental Biology, University of Connecticut Health Center, Farmington, CT, USA.
Liu T; Center for Advanced Proteomic Research, Rutgers Biomedical and Health Sciences, Newark, NJ, USA.
Li H; Center for Advanced Proteomic Research, Rutgers Biomedical and Health Sciences, Newark, NJ, USA.
Kalodimos CG; Department of Chemistry and Chemical Biology, Rutgers University, Piscataway, NJ, USA.
Birge RB; Department of Biochemistry and Molecular Biology, Rutgers Biomedical and Health Sciences, Newark, NJ, USA.
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Źródło:
Oncogene [Oncogene] 2015 Aug 06; Vol. 34 (32), pp. 4260-9. Date of Electronic Publication: 2014 Nov 10.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural
MeSH Terms:
Signal Transduction*
src Homology Domains*
Proto-Oncogene Proteins c-crk/*metabolism
Tyrosine/*metabolism
Amino Acid Sequence ; Animals ; Blotting, Western ; Cell Line, Tumor ; Chromatography, Liquid ; HEK293 Cells ; Humans ; Mice ; Molecular Sequence Data ; NIH 3T3 Cells ; Oncogene Proteins v-abl/metabolism ; Phosphorylation ; Protein Binding ; Proto-Oncogene Proteins c-crk/genetics ; Sequence Homology, Amino Acid ; Tandem Mass Spectrometry ; Tyrosine/genetics
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
Loss of giant obscurins from breast epithelium promotes epithelial-to-mesenchymal transition, tumorigenicity and metastasis.
Autorzy:
Shriver M; Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD, USA.
Stroka KM; 1] Department of Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, MD, USA [2] Johns Hopkins Institute for NanoBioTechnology, The Johns Hopkins University, Baltimore, MD, USA [3] Johns Hopkins Physical Sciences-Oncology Center, The Johns Hopkins University, Baltimore, MD, USA.
Vitolo MI; Marlene and Stewart Greenebaum National Cancer Institute Cancer Center, University of Maryland School of Medicine, Baltimore, MD, USA.
Martin S; Marlene and Stewart Greenebaum National Cancer Institute Cancer Center, University of Maryland School of Medicine, Baltimore, MD, USA.
Huso DL; Department of Molecular and Comparative Pathobiology, The Johns Hopkins University and The Sidney Kimmel Comprehensive Cancer Center, Baltimore, MD, USA.
Konstantopoulos K; 1] Department of Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, MD, USA [2] Johns Hopkins Institute for NanoBioTechnology, The Johns Hopkins University, Baltimore, MD, USA [3] Johns Hopkins Physical Sciences-Oncology Center, The Johns Hopkins University, Baltimore, MD, USA.
Kontrogianni-Konstantopoulos A; 1] Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD, USA [2] Marlene and Stewart Greenebaum National Cancer Institute Cancer Center, University of Maryland School of Medicine, Baltimore, MD, USA.
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Źródło:
Oncogene [Oncogene] 2015 Aug 06; Vol. 34 (32), pp. 4248-59. Date of Electronic Publication: 2014 Nov 10.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural
MeSH Terms:
Breast/*metabolism
Cell Transformation, Neoplastic/*genetics
Epithelial-Mesenchymal Transition/*genetics
Rho Guanine Nucleotide Exchange Factors/*genetics
Biopsy ; Blotting, Western ; Breast/pathology ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cadherins/genetics ; Cadherins/metabolism ; Cell Adhesion/genetics ; Cell Line ; Cell Movement/genetics ; Cell Transformation, Neoplastic/metabolism ; Epithelial Cells/metabolism ; Epithelium/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Intercellular Junctions/metabolism ; Microscopy, Confocal ; Neoplasm Metastasis ; Protein Serine-Threonine Kinases ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins p21(ras) ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Rho Guanine Nucleotide Exchange Factors/metabolism ; Transplantation, Heterologous ; Vimentin/genetics ; Vimentin/metabolism ; ras Proteins/genetics ; ras Proteins/metabolism
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
The human oncoprotein and chromatin architectural factor DEK counteracts DNA replication stress.
Autorzy:
Deutzmann A; Bioimaging Center, Department of Biology, University of Konstanz, Konstanz, Germany.
Ganz M; Bioimaging Center, Department of Biology, University of Konstanz, Konstanz, Germany.
Schönenberger F; Bioimaging Center, Department of Biology, University of Konstanz, Konstanz, Germany.
Vervoorts J; Institute of Biochemistry and Molecular Biology, Medical School, RWTH Aachen University, Aachen, Germany.
Kappes F; Institute of Biochemistry and Molecular Biology, Medical School, RWTH Aachen University, Aachen, Germany.
Ferrando-May E; Bioimaging Center, Department of Biology, University of Konstanz, Konstanz, Germany.
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Źródło:
Oncogene [Oncogene] 2015 Aug 06; Vol. 34 (32), pp. 4270-7. Date of Electronic Publication: 2014 Oct 27.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:
DNA Replication*
Chromatin/*genetics
Chromosomal Proteins, Non-Histone/*genetics
Oncogene Proteins/*genetics
Aphidicolin/pharmacology ; Blotting, Western ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Proliferation/genetics ; Cell Survival/drug effects ; Cell Survival/genetics ; Chromatin/metabolism ; Chromosomal Proteins, Non-Histone/metabolism ; DNA Damage ; Dose-Response Relationship, Drug ; Enzyme Inhibitors/pharmacology ; HeLa Cells ; Humans ; Hydroxyurea/pharmacology ; Microscopy, Fluorescence ; Oncogene Proteins/metabolism ; Poly-ADP-Ribose Binding Proteins ; RNA Interference
Czasopismo naukowe
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Tytuł:
Anti-angiogenic pathway associations of the 3p21.3 mapped BLU gene in nasopharyngeal carcinoma.
Autorzy:
Cheng Y; Department of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
Ho RL; Department of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
Chan KC; Department of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
Kan R; Department of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
Tung E; Department of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
Lung HL; Department of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
Yau WL; Department of Anatomical and Cellular Pathology, Chinese University of Hong Kong, Hong Kong, SAR, Hong Kong.
Cheung AK; Department of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
Ko JM; Department of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
Zhang ZF; Department of Pathology, Guangxi Medical University, Guangxi, People's Republic of China.
Luo DZ; Department of Pathology, Guangxi Medical University, Guangxi, People's Republic of China.
Feng ZB; Department of Pathology, Guangxi Medical University, Guangxi, People's Republic of China.
Chen S; Department of Pathology, Guangxi Medical University, Guangxi, People's Republic of China.
Guan XY; Department of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
Kwong D; Department of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
Stanbridge EJ; Department of Microbiology and Molecular Genetics, University of California, Irvine, CA, USA.
Lung ML; Department of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
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Źródło:
Oncogene [Oncogene] 2015 Aug 06; Vol. 34 (32), pp. 4219-28. Date of Electronic Publication: 2014 Oct 27.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:
Chromosomes, Human, Pair 3/*genetics
Nasopharyngeal Neoplasms/*genetics
Neovascularization, Pathologic/*genetics
Signal Transduction/*genetics
Tumor Suppressor Proteins/*genetics
Animals ; Blotting, Western ; Carcinoma ; Cell Line, Tumor ; Cell Movement/genetics ; Cells, Cultured ; Chromosome Mapping ; Cytoskeletal Proteins ; Down-Regulation ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Immunohistochemistry ; Male ; Matrix Metalloproteinases/genetics ; Matrix Metalloproteinases/metabolism ; Mice, Nude ; Nasopharyngeal Carcinoma ; Nasopharyngeal Neoplasms/metabolism ; Nasopharyngeal Neoplasms/pathology ; Reverse Transcriptase Polymerase Chain Reaction ; Thrombospondin 1/genetics ; Thrombospondin 1/metabolism ; Transplantation, Heterologous ; Tumor Microenvironment/genetics ; Tumor Suppressor Proteins/metabolism ; Vascular Endothelial Growth Factor A/genetics ; Vascular Endothelial Growth Factor A/metabolism
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
LKB1 reduces ROS-mediated cell damage via activation of p38.
Autorzy:
Xu HG; Division of Hematology and Oncology, Department of Medicine, Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA.
Zhai YX; Key Laboratory of Pathobiology, Ministry of Education, Department of Pathology, Norman Bethune College of Medicine, Jilin University, Changchun, China.
Chen J; Division of Hematology and Oncology, Department of Medicine, Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA.
Lu Y; Department of Endocrinology, the Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Wang JW; Key Laboratory of Pathobiology, Ministry of Education, Department of Pathology, Norman Bethune College of Medicine, Jilin University, Changchun, China.
Quan CS; Key Laboratory of Pathobiology, Ministry of Education, Department of Pathology, Norman Bethune College of Medicine, Jilin University, Changchun, China.
Zhao RX; Division of Hematology and Oncology, Department of Medicine, Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA.
Xiao X; Division of Hematology and Oncology, Department of Medicine, Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA.
He Q; Division of Hematology and Oncology, Department of Medicine, Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA.
Werle KD; Division of Hematology and Oncology, Department of Medicine, Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA.
Kim HG; Division of Hematology and Oncology, Department of Medicine, Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA.
Lopez R; Division of Hematology and Oncology, Department of Medicine, Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA.
Cui R; Department of Dermatology, Boston University, School of Medicine, Boston, MA, USA.
Liang J; Department of Systems Biology, UT MD Anderson Cancer Center, Houston, TX, USA.
Li YL; Key Laboratory of Pathobiology, Ministry of Education, Department of Pathology, Norman Bethune College of Medicine, Jilin University, Changchun, China.
Xu ZX; 1] Division of Hematology and Oncology, Department of Medicine, Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA [2] Key Laboratory of Pathobiology, Ministry of Education, Department of Pathology, Norman Bethune College of Medicine, Jilin University, Changchun, China.
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Źródło:
Oncogene [Oncogene] 2015 Jul; Vol. 34 (29), pp. 3848-59. Date of Electronic Publication: 2014 Sep 29.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
MeSH Terms:
DNA Damage*
Protein Serine-Threonine Kinases/*metabolism
Reactive Oxygen Species/*metabolism
p38 Mitogen-Activated Protein Kinases/*metabolism
AMP-Activated Protein Kinase Kinases ; AMP-Activated Protein Kinases ; Acetylcysteine/pharmacology ; Activating Transcription Factor 2/metabolism ; Animals ; Blotting, Western ; Catalase/metabolism ; Cell Line, Tumor ; Cells, Cultured ; Embryo, Mammalian/cytology ; Enzyme Activation/drug effects ; Fibroblasts/metabolism ; Free Radical Scavengers/pharmacology ; HeLa Cells ; Humans ; Mice, Knockout ; Microscopy, Fluorescence ; Protein Binding/drug effects ; Protein Serine-Threonine Kinases/genetics ; RNA Interference ; Superoxide Dismutase/metabolism ; cdc42 GTP-Binding Protein/metabolism ; p21-Activated Kinases/metabolism
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
Anticipatory estrogen activation of the unfolded protein response is linked to cell proliferation and poor survival in estrogen receptor α-positive breast cancer.
Autorzy:
Andruska N; 1] Department of Biochemistry, University of Illinois, Urbana, IL, USA [2] College of Medicine, University of Illinois, Urbana, IL, USA.
Zheng X; Department of Biochemistry, University of Illinois, Urbana, IL, USA.
Yang X; Department of Food Science and Human Nutrition, University of Illinois, Urbana, IL, USA.
Helferich WG; 1] College of Medicine, University of Illinois, Urbana, IL, USA [2] Department of Food Science and Human Nutrition, University of Illinois, Urbana, IL, USA [3] University of Illinois Cancer Center, Urbana, IL, USA.
Shapiro DJ; 1] Department of Biochemistry, University of Illinois, Urbana, IL, USA [2] College of Medicine, University of Illinois, Urbana, IL, USA [3] University of Illinois Cancer Center, Urbana, IL, USA.
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Źródło:
Oncogene [Oncogene] 2015 Jul; Vol. 34 (29), pp. 3760-9. Date of Electronic Publication: 2014 Sep 29.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
MeSH Terms:
Breast Neoplasms/*metabolism
Cell Proliferation/*drug effects
Estradiol/*pharmacology
Estrogen Receptor alpha/*metabolism
Unfolded Protein Response/*drug effects
Animals ; Antineoplastic Agents, Hormonal/therapeutic use ; Blotting, Western ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Cell Line, Tumor ; Cell Proliferation/genetics ; Endoplasmic Reticulum Chaperone BiP ; Estrogen Receptor alpha/genetics ; Estrogens/pharmacology ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic/drug effects ; Heat-Shock Proteins/genetics ; Heat-Shock Proteins/metabolism ; Humans ; Kaplan-Meier Estimate ; MCF-7 Cells ; Mice, Nude ; Microscopy, Confocal ; Oligonucleotide Array Sequence Analysis ; Ovariectomy ; RNA Interference ; Reverse Transcriptase Polymerase Chain Reaction ; Tamoxifen/therapeutic use ; Transplantation, Heterologous ; Unfolded Protein Response/genetics
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
Myeloid zinc-finger 1 (MZF-1) suppresses prostate tumor growth through enforcing ferroportin-conducted iron egress.
Autorzy:
Chen Y; 1] Department of Urology, The Second Hospital of Tianjin Medical University, Tianjin Institute of Urology, Tianjin, China [2] State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing, China.
Zhang Z; Department of Urology, The Second Hospital of Tianjin Medical University, Tianjin Institute of Urology, Tianjin, China.
Yang K; Department of Urology, The Second Hospital of Tianjin Medical University, Tianjin Institute of Urology, Tianjin, China.
Du J; School of Life Sciences, Tsinghua University, Beijing, China.
Xu Y; Department of Urology, The Second Hospital of Tianjin Medical University, Tianjin Institute of Urology, Tianjin, China.
Liu S; State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing, China.
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Źródło:
Oncogene [Oncogene] 2015 Jul; Vol. 34 (29), pp. 3839-47. Date of Electronic Publication: 2014 Oct 06.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
MeSH Terms:
Cation Transport Proteins/*metabolism
Iron/*metabolism
Kruppel-Like Transcription Factors/*metabolism
Prostatic Neoplasms/*metabolism
3' Untranslated Regions/genetics ; Animals ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Blotting, Western ; Cation Transport Proteins/genetics ; Cell Line, Tumor ; Cell Proliferation/genetics ; Cell Survival/genetics ; DNA-Binding Proteins ; Ferritins/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Kruppel-Like Transcription Factors/genetics ; Male ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology ; Proto-Oncogene Proteins c-myb/genetics ; Proto-Oncogene Proteins c-myb/metabolism ; RNA Interference ; RNA-Binding Proteins ; Reverse Transcriptase Polymerase Chain Reaction ; Transplantation, Heterologous ; Tumor Burden/genetics
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
Tytuł:
Survivin as a therapeutic target in Sonic hedgehog-driven medulloblastoma.
Autorzy:
Brun SN; 1] Tumor Initiation and Maintenance Program, National Cancer Institute (NCI)-Designated Cancer Center, Sanford-Burnham Medical Research Institute (SBMRI), La Jolla, CA, USA [2] Sanford Consortium for Regenerative Medicine, La Jolla, CA, USA [3] Department of Pharmacology and Cancer Biology, Duke University, Durham, NC, USA.
Markant SL; 1] Tumor Initiation and Maintenance Program, National Cancer Institute (NCI)-Designated Cancer Center, Sanford-Burnham Medical Research Institute (SBMRI), La Jolla, CA, USA [2] Sanford Consortium for Regenerative Medicine, La Jolla, CA, USA [3] Department of Pharmacology and Cancer Biology, Duke University, Durham, NC, USA.
Esparza LA; 1] Tumor Initiation and Maintenance Program, National Cancer Institute (NCI)-Designated Cancer Center, Sanford-Burnham Medical Research Institute (SBMRI), La Jolla, CA, USA [2] Sanford Consortium for Regenerative Medicine, La Jolla, CA, USA.
Garcia G; Histopathology Core SBMRI, La Jolla, CA, USA.
Terry D; Conrad Prebys Center for Chemical Genomics, SBMRI, Lake Nona, FL, USA.
Huang JM; Cedars-Sinai Women's Cancer Program at the Samuel Oschin Comprehensive Cancer Institute, Los Angeles, CA, USA.
Pavlyukov MS; 1] Department of Neurological Surgery, The Ohio State University, Columbus, OH, USA [2] James Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
Li XN; Brain Tumor Program, Texas Children's Cancer Center, and Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA.
Grant GA; Department of Neurosurgery, Stanford University/Lucile Packard Children's Hospital, Stanford, CA, USA.
Crawford JR; 1] Department of Pediatrics, University of California San Diego, San Diego, CA, USA [2] Departments of Neurosciences, University of California San Diego, San Diego, CA, USA [3] Rady Children's Hospital, San Diego, CA, USA.
Levy ML; 1] Rady Children's Hospital, San Diego, CA, USA [2] Department of Neurosurgery, University of California San Diego, La Jolla, CA, USA.
Conway EM; Centre for Blood Research, Division of Hematology, Department of Medicine, University of British Columbia (UBC), Vancouver, BC, Canada.
Smith LH; 1] Conrad Prebys Center for Chemical Genomics, SBMRI, Lake Nona, FL, USA [2] Cardiopathobiology Program, Sanford Burnham Medical Research Institute, Lake Nona, FL, USA.
Nakano I; 1] Department of Neurological Surgery, The Ohio State University, Columbus, OH, USA [2] James Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
Berezov A; Department of Biomedical Sciences at Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Greene MI; Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Wang Q; Cedars-Sinai Women's Cancer Program at the Samuel Oschin Comprehensive Cancer Institute, Los Angeles, CA, USA.
Wechsler-Reya RJ; 1] Tumor Initiation and Maintenance Program, National Cancer Institute (NCI)-Designated Cancer Center, Sanford-Burnham Medical Research Institute (SBMRI), La Jolla, CA, USA [2] Sanford Consortium for Regenerative Medicine, La Jolla, CA, USA [3] Department of Pharmacology and Cancer Biology, Duke University, Durham, NC, USA.
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Źródło:
Oncogene [Oncogene] 2015 Jul; Vol. 34 (29), pp. 3770-9. Date of Electronic Publication: 2014 Sep 22.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
MeSH Terms:
Cerebellar Neoplasms/*metabolism
Hedgehog Proteins/*metabolism
Inhibitor of Apoptosis Proteins/*deficiency
Medulloblastoma/*metabolism
Repressor Proteins/*deficiency
Animals ; Apoptosis/drug effects ; Apoptosis/radiation effects ; Biphenyl Compounds/pharmacology ; Blotting, Western ; Cell Cycle/drug effects ; Cell Cycle/radiation effects ; Cell Proliferation/drug effects ; Cell Proliferation/radiation effects ; Cerebellar Neoplasms/drug therapy ; Cerebellar Neoplasms/genetics ; Chemoradiotherapy ; Child ; Hedgehog Proteins/antagonists & inhibitors ; Humans ; Imidazoles/pharmacology ; Inhibitor of Apoptosis Proteins/antagonists & inhibitors ; Inhibitor of Apoptosis Proteins/genetics ; Interleukin Receptor Common gamma Subunit/deficiency ; Interleukin Receptor Common gamma Subunit/genetics ; Ki-67 Antigen/metabolism ; Medulloblastoma/drug therapy ; Medulloblastoma/genetics ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, Knockout ; Mice, Nude ; Mice, SCID ; Microscopy, Confocal ; Naphthoquinones/pharmacology ; Pyridines/pharmacology ; Repressor Proteins/antagonists & inhibitors ; Repressor Proteins/genetics ; Survivin ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Czasopismo naukowe
Pełny tekst  Link otwiera się w nowym oknieSzczegóły
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