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Long non-coding RNA AFAP1-AS1 promotes proliferation and migration of gastric cancer by downregulating KLF2

X-H Yuan1, J Li, Y Cao

  • 1Department of General Surgery, Jiangxi provincial People's Hospital Affiliated to Nanchang University, Nanchang, Chinajiezg123@126.com.

European Review for Medical and Pharmacological Sciences
|February 5, 2020
PubMed
Abstract

Insights

Actin filament associated protein 1-antisense RNA1 (AFAP1-AS1) promotes gastric cancer (GC) progression by increasing cell proliferation and migration. This long non-coding RNA (lncRNA) downregulates Krüppel-like factor 2 (KLF2) expression, driving GC advancement.

Area of Science:

  • Molecular Oncology
  • Cancer Biology
  • Epigenetics

Background:

  • Gastric cancer (GC) remains a significant global health challenge.
  • Understanding the molecular mechanisms driving GC progression is crucial for developing targeted therapies.
  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer development.

Purpose of the Study:

  • To elucidate the function of actin filament associated protein 1-antisense RNA1 (AFAP1-AS1) in gastric cancer (GC) cell proliferation and migration.
  • To investigate the regulatory relationship between AFAP1-AS1 and Krüppel-like factor 2 (KLF2) in GC.
  • To explore the underlying molecular mechanisms by which AFAP1-AS1 influences GC progression.

Main Methods:

  • Quantitative real-time polymerase chain reaction (qRT-PCR) to assess AFAP1-AS1 expression in GC tissues.
  • Functional experiments (e.g., knockdown) to evaluate AFAP1-AS1's role in GC cell behavior.
  • Chromatin immunoprecipitation (ChIP) assay to determine AFAP1-AS1's interaction with EZH2.
  • Western blot to detect KLF2 expression changes influenced by AFAP1-AS1 and EZH2.

Main Results:

  • AFAP1-AS1 was significantly upregulated in GC tissues, particularly in cases with lymph node metastasis and advanced stages.
  • Knockdown of AFAP1-AS1 inhibited GC cell viability, proliferation, and migration, while inducing apoptosis.
  • AFAP1-AS1 was found to bind to EZH2, and its knockdown attenuated EZH2 recruitment.
  • Both AFAP1-AS1 and EZH2 knockdown led to increased KLF2 expression, and KLF2 knockdown partially reversed AFAP1-AS1's effects on GC cells.

Conclusions:

  • Long non-coding RNA AFAP1-AS1 promotes GC cell proliferation and migration by downregulating KLF2 expression.
  • The AFAP1-AS1/EZH2 axis plays a critical role in regulating KLF2 levels and subsequently promoting GC progression.
  • Targeting AFAP1-AS1 may represent a potential therapeutic strategy for gastric cancer.

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