Environmental toxicology, 2021-07, Vol.36 (7), p.1278-1287
2021
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- Autor(en) / Beteiligte
- Titel
- AXL is crucial for E1A‐enhanced therapeutic efficiency of EGFR tyrosine kinase inhibitors through NFI in breast cancer
- Ist Teil von
- Environmental toxicology, 2021-07, Vol.36 (7), p.1278-1287
- Ort / Verlag
- Hoboken, USA: John Wiley & Sons, Inc
- Erscheinungsjahr
- 2021
- Quelle
- Wiley-Blackwell Journals
- Beschreibungen/Notizen
- 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.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1520-4081eISSN: 1522-7278DOI: 10.1002/tox.23125Titel-ID: cdi_proquest_miscellaneous_2502809764
- Format
- –
- Schlagworte
- AXL, Axl protein, Breast cancer, Breast Neoplasms - drug therapy, Breast Neoplasms - genetics, Cancer, Cell death, Cell Line, Tumor, Drug Resistance, Neoplasm, Early region, EGFR tyrosine kinase inhibitor, Enzyme inhibitors, Epidermal growth factor, Epidermal growth factor receptors, ErbB Receptors - genetics, Growth factors, Humans, Kinases, Neoplasms, NFI Transcription Factors, Nuclear factor I, Protein Kinase Inhibitors - pharmacology, Protein Kinase Inhibitors - therapeutic use, Proto-Oncogene Proteins - genetics, Receptor Protein-Tyrosine Kinases - genetics, Survival, Transcription, Tyrosine, Tyrosine kinase inhibitors