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AXL transcriptionally up-regulates TMEM14A expression to mediate cell proliferation in non-small-cell lung cancer

Te-Hsuan Jang1, Sheng-Chieh Lin1, Ya-Yu Yang1

  • 1National Institute of Cancer Research, National Health Research Institutes, Miaoli, Taiwan.

Biochemical and Biophysical Research Communications
|October 15, 2023
PubMed

Insights

This study identifies TMEM14A as a key gene regulated by AXL in non-small cell lung cancer (NSCLC). Increased TMEM14A expression correlates with poorer survival, suggesting it as a potential therapeutic target for NSCLC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • AXL receptor tyrosine kinase drives non-small cell lung cancer (NSCLC) progression and therapy resistance.
  • The precise molecular mechanisms of AXL-driven oncogenesis in NSCLC are not fully understood.

Purpose of the Study:

  • To identify downstream genes regulated by AXL in NSCLC.
  • To investigate the role of TMEM14A in NSCLC pathogenesis and its relationship with AXL signaling.

Main Methods:

  • Transcriptomic RNA sequencing of AXL-silenced NSCLC cells.
  • Bioinformatic analysis using GEPIA2 for clinical correlation.
  • Experimental validation of TMEM14A function via gene silencing.
  • Promoter analysis to elucidate regulatory mechanisms.

Main Results:

  • TMEM14A was identified as a significantly upregulated gene upon AXL silencing in NSCLC cells.
  • Elevated TMEM14A mRNA expression observed in lung adenocarcinoma (LUAD) tissues, correlating with reduced overall survival.
  • Silencing TMEM14A inhibited NSCLC cell proliferation and ATP levels.
  • AXL-mediated TMEM14A transcription potentially involves STAT and NF-κB transcription factors.

Conclusions:

  • TMEM14A is a novel downstream target of AXL in NSCLC.
  • TMEM14A plays a crucial role in NSCLC progression and may serve as a biomarker for patient prognosis.
  • Targeting TMEM14A presents a potential therapeutic strategy to overcome AXL-driven resistance in NSCLC.
Keywords:
ATP productionAXLCell proliferationNSCLCTMEM14ATranscriptional regulation

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