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

Chih Ming Su, Tung Wei Hsu, Shian Ying Sung, Ming Te Huang, Kuan Chou Chen, Chih Yang Huang, Chien Yi Chiang, Yen Hao Su, Hsin An Chen, Po Hsiang Liao

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)1278-1287
Number of pages10
JournalEnvironmental Toxicology
Volume36
Issue number7
DOIs
Publication statusAccepted/In press - 2021

Keywords

  • AXL
  • breast cancer
  • EGFR tyrosine kinase inhibitor
  • nuclear factor I

ASJC Scopus subject areas

  • Toxicology
  • Management, Monitoring, Policy and Law
  • Health, Toxicology and Mutagenesis

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