AXL is crucial for E1A-enhanced therapeutic efficiency of EGFR tyrosine kinase inhibitors through NFI in breast cancer.

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Abstrakt

Tytuł:: AXL is crucial for E1A-enhanced therapeutic efficiency of EGFR tyrosine kinase inhibitors through NFI in breast cancer.
Autorzy:: Su CM; Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei City, Taiwan.; Division of General Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.; Graduate Institute of Clinical Medicine, College of Medicine Taipei Medical University, Taipei City, Taiwan.
Hsu TW; Division of General Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.; Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei City, Taiwan.
Sung SY; Ph.D. Program for Translational Medicine, College of Medical Science and Technology, Taipei Medical University, New Taipei City, Taiwan.
Huang MT; Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei City, Taiwan.; Division of General Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.; Graduate Institute of Clinical Medicine, College of Medicine Taipei Medical University, Taipei City, Taiwan.
Chen KC; Department of sport and physical education, Hong Kong Baptist University, Kowloon Tong, Hong Kong.
Huang CY; Cardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.; Center of General Education, Buddhist Tzu Chi Medical Foundation, Tzu Chi University of Science and Technology, Hualien, Taiwan.; Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, Taiwan.; Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.
Chiang CY; Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, Taiwan.
Su YH; Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei City, Taiwan.; Division of General Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.; Graduate Institute of Clinical Medicine, College of Medicine Taipei Medical University, Taipei City, Taiwan.
Chen HA; Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei City, Taiwan.; Division of General Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.; Graduate Institute of Clinical Medicine, College of Medicine Taipei Medical University, Taipei City, Taiwan.
Liao PH; Division of General Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
Źródło:: Environmental toxicology [Environ Toxicol] 2021 Jul; Vol. 36 (7), pp. 1278-1287. Date of Electronic Publication: 2021 Mar 18.
Typ publikacji:: Journal Article
Język:: English
Imprint Name(s):: Original Publication: New York, NY : John Wiley & Sons, c1999-
MeSH Terms:: Breast Neoplasms*/drug therapy
Breast Neoplasms*/genetics
Receptor Protein-Tyrosine Kinases*/genetics
Cell Line, Tumor ; Drug Resistance, Neoplasm ; ErbB Receptors/genetics ; Humans ; NFI Transcription Factors ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Proto-Oncogene Proteins/genetics ; Axl Receptor Tyrosine Kinase
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Grant Information:: MOST108-2314-B-038-109 Ministry of Science and Technology grants from Taiwan; MOST 109-2320-B-038 -043 Ministry of Science and Technology grants from Taiwan; 103TMU-SHH-26 Taipei Medical University-Shuang Ho Hospital, Ministry of Health and Welfare grant from Taiwan; 104TMU-SHH-01-1 Taipei Medical University-Shuang Ho Hospital, Ministry of Health and Welfare grant from Taiwan; DP2-110-21121-03-C-08-03 TMU Research Center of Cancer Translational Medicine from The Featured Areas Research Center Program within the framework of the Higher Education Sprout Project by the Ministry of Education (MOE) in Taiwan; DP2-110-21121-03-C-08-01 TMU Research Center of Cancer Translational Medicine from The Featured Areas Research Center Program within the framework of the Higher Education Sprout Project by the Ministry of Education (MOE) in Taiwan
Contributed Indexing:: Keywords: AXL; EGFR tyrosine kinase inhibitor; breast cancer; nuclear factor I
Substance Nomenclature:: 0 (NFI Transcription Factors)
0 (Protein Kinase Inhibitors)
0 (Proto-Oncogene Proteins)
EC 2.7.10.1 (EGFR protein, human)
EC 2.7.10.1 (ErbB Receptors)
EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
0 (Axl Receptor Tyrosine Kinase)
0 (AXL protein, human)
Entry Date(s):: Date Created: 20210318 Date Completed: 20210604 Latest Revision: 20221207
Update Code:: 20240105
DOI:: 10.1002/tox.23125
PMID:: 33734566
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AXL which is a chemosensitizer protein for breast cancer cells in response to epidermal growth factor receptor-tyrosine kinase inhibitor and suppresses tumor growth. The clinical information show nuclear factor I (NFI)-C and NFI-X expression correlate with AXL expression in breast cancer patients. Following, we establish serial deletions of AXL promoter to identify regions required for Adenovirus-5 early region 1A (E1A)-mediated AXL suppression. All of the NFI family members were extensively studied for their expression and functions in regulating AXL. Moreover, E1A post-transcriptionally downregulates AXL expression through NFI. NFI-C and NFI-X, not NFI-A and NFI-B, resulting in cell death in response to EGFR-TKI. Our finding suggests that NFI-C and NFI-X are crucial regulators for AXL and significantly correlated with poor survival of breast cancer patients.
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