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AFAP1-AS1 induces cisplatin resistance in non-small cell lung cancer through PI3K/AKT pathway

Yang Liu1, Qiang Hu2, Xihui Wang3

  • 1Department of Pharmacy, Linyi Central Hospital, Linyi, Shandong 276400, P.R. China.

Oncology Letters
|January 4, 2020
PubMed

Insights

AFAP1-AS1 promotes cisplatin resistance in non-small cell lung cancer (NSCLC) by interacting with EZH2 to activate the PI3K/AKT pathway. This interaction enhances tumor cell proliferation and metastasis while inhibiting apoptosis in NSCLC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Cisplatin (DDP) resistance significantly impacts non-small cell lung cancer (NSCLC) patient outcomes.
  • Understanding the molecular mechanisms underlying DDP resistance is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of AFAP1-AS1 in DDP-resistant NSCLC.
  • To elucidate the underlying molecular mechanisms involving AFAP1-AS1 in DDP resistance.

Main Methods:

  • Quantified AFAP1-AS1 expression in DDP-resistant NSCLC tissues and cells.
  • Assessed cellular changes (proliferation, apoptosis, migration, invasion) after si-AFAP1-AS1 transfection.
  • Utilized Western blot to analyze key protein levels (p-AKT, AKT, E-cadherin, N-cadherin, vimentin, snail).
  • Performed RNA immunoprecipitation (RIP) assay to confirm AFAP1-AS1 and EZH2 interaction.
  • Investigated EZH2's effect on the PI3K/AKT pathway.

Main Results:

  • AFAP1-AS1 was significantly upregulated in DDP-resistant NSCLC and cells (A549/DDP).
  • Silencing AFAP1-AS1 reduced proliferation, migration, and invasion, arrested cell cycle, and induced apoptosis.
  • AFAP1-AS1 directly interacted with EZH2, and AFAP1-AS1 upregulation correlated with EZH2 expression.
  • Silencing AFAP1-AS1 or EZH2 inhibited the PI3K/AKT pathway activation.

Conclusions:

  • AFAP1-AS1 promotes proliferation and metastasis while inhibiting apoptosis in DDP-resistant NSCLC cells.
  • AFAP1-AS1 induces DDP resistance by interacting with EZH2 to activate the PI3K/AKT pathway.
  • AFAP1-AS1 represents a potential therapeutic target for overcoming DDP resistance in NSCLC.
Keywords:
AFAP1-AS1PI3K/AKTcisplatin resistancenon-small cell lung carcinoma

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