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Tytuł pozycji:

BRCA1-associated protein inhibits glioma cell proliferation and migration and glioma stem cell self-renewal via the TGF-β/PI3K/AKT/mTOR signalling pathway.

Tytuł:
BRCA1-associated protein inhibits glioma cell proliferation and migration and glioma stem cell self-renewal via the TGF-β/PI3K/AKT/mTOR signalling pathway.
Autorzy:
Wang B; Department of Neurosurgery, Tianjin Huanhu Hospital; Tianjin Key Laboratory of Cerebral Vascular and Neurodegenerative diseases, Tianjin Neurosurgical Institute, No. 6 Jizhao Road, Tianjin, 300350, China.; State Key Laboratory of Medicinal Chemical Biology, Nankai University, No.94 Weijin Road, Tianjin, 300071, China.
Cao C; Department of Medical Imaging, Tianjin Huanhu Hospital; Tianjin Key Laboratory of Cerebral Vascular and Neurodegenerative diseases, Tianjin Neurosurgical Institute, No. 6 Jizhao Road, Tianjin, 300350, China.
Liu X; Department of Gastroenterology, Tianjin Nankai Hospital, No.6 Changjiang Road, Tianjin, 300100, China.
He X; Department of Biological Sciences, Virginia Tech, Blacksburg, VA, 24061, USA.
Zhuang H; Department of Hepatic Biliary Pancreatic Surgery, Cancer Hospital Affiliated to Zhengzhou University, Zhengzhou, 450008, Henan Province, China. .
Wang D; Department of Neurosurgery, General Hospital; Tianjin Key Laboratory of Injuries, Variations, and Regeneration of Nervous System; Tianjin Neurological Institute, Tianjin Medical University, No.154 Anshan Road, Tianjin, 300052, China. .
Chen B; Department of Neurosurgery, Tianjin Huanhu Hospital; Tianjin Key Laboratory of Cerebral Vascular and Neurodegenerative diseases, Tianjin Neurosurgical Institute, No. 6 Jizhao Road, Tianjin, 300350, China. .
Źródło:
Cellular oncology (Dordrecht) [Cell Oncol (Dordr)] 2020 Apr; Vol. 43 (2), pp. 223-235. Date of Electronic Publication: 2019 Nov 27.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Original Publication: Dordrecht : Springer
MeSH Terms:
Cell Movement/*genetics
Cell Proliferation/*genetics
Glioma/*genetics
Neoplastic Stem Cells/*metabolism
Proteins/*metabolism
Ubiquitin-Protein Ligases/*genetics
Animals ; Cell Line, Tumor ; Cell Self Renewal ; Female ; Gene Expression Regulation, Neoplastic ; Glioma/metabolism ; Glioma/therapy ; Humans ; Kaplan-Meier Estimate ; Male ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; RNA Interference ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism ; Transforming Growth Factor beta/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Xenograft Model Antitumor Assays
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Grant Information:
2018048 Open Project of State Key Laboratory of Medicinal Chemical Biology, Nankai University; 63191106 Fundamental Research Funds for the Central Universities, Nankai University; 81671380 Chinese National Natural Science Foundation; 81573737 Chinese National Natural Science Foundation; 17JCZDJC35900 Key Project of Tianjin National Natural Science Foundation; 172102310103 Science and Technology Development Foundation of Henan Province; 2018020480 Henan Provincial Medical Science and Technology Project; 81902477 National Natural Science Foundation of China
Contributed Indexing:
Keywords: BRAP; Cancer stem cells; Glioma; mTOR
Substance Nomenclature:
0 (Proteins)
0 (Transforming Growth Factor beta)
EC 2.3.2.27 (BRAP protein, human)
EC 2.3.2.27 (Ubiquitin-Protein Ligases)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
EC 2.7.11.1 (TOR Serine-Threonine Kinases)
Entry Date(s):
Date Created: 20191129 Date Completed: 20201207 Latest Revision: 20211204
Update Code:
20240104
DOI:
10.1007/s13402-019-00482-8
PMID:
31776938
Czasopismo naukowe
Purpose: BRCA1-associated protein (BRAP) was first identified by its ability to bind to the nuclear localization signalling motif of BRCA1 and other proteins. Subsequently, human BRAP has been found to exert multiple functions, many of which are related to cancer development. Up till now, however, the role of BRAP in glioma development has remained obscure. Here, we report a role for BRAP in mediating the proliferation and migration of glioma cells both in vitro and in vivo.
Methods: The expression of BRAP in 98 glioma patient samples was determined by immunohistochemistry, after which associations between BRAP expression and patient prognosis were assessed. A short hairpin RNA (shRNA) was used to knock down BRAP and an expression vector was used to exogenously overexpress BRAP in glioma cells. The effects of BRAP expression on tumour cell behaviour in vitro and in an in vivo xenograft mouse model were examined.
Results: We found that in glioma patients BRAP expression was associated with a favourable prognosis. We also found that shRNA-mediated knockdown of BRAP facilitated the proliferation and migration of glioma cells and the self-renewal of glioma stem cells. In parallel, we found that BRAP knockdown increased tumour growth and invasion and decreased survival in an in vivo glioma xenograft mouse model. Mechanistically, we found that BRAP inhibited glioma cell proliferation and migration, as well as glioma stem cell self-renewal via the TGF-β/PI3K/AKT/mTOR signalling pathway.
Conclusions: Together, our findings identify BRAP as a mediator of glioma cell proliferation, migration and glioma stem cell self-renewal.
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