Long non-coding RNA AFAP1-AS1 promotes proliferation and invasion in prostate cancer via targeting miR-512-3p

Kai Wang1, Hao Sun2, Tao Sun3

  • 1Urology Department, Liaoning Cancer Hospital & Institute, Cancer Hospital of China Medical University, Shengyang City, Liaoning Province 110044, PR China.

Gene
|November 1, 2019
PubMed
Abstract

Insights

Long non-coding RNA AFAP1-AS1 promotes prostate cancer progression by regulating miR-512-3p. Silencing AFAP1-AS1 inhibits cell proliferation and migration, offering therapeutic potential for prostate cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • Prostate cancer remains a significant health concern with ongoing research into novel therapeutic targets.
  • The role of long non-coding RNAs (lncRNAs) in cancer development is increasingly recognized, yet the specific function of AFAP1-AS1 in prostate cancer is unclear.

Purpose of the Study:

  • To investigate the role of lncRNA AFAP1-AS1 in the pathogenesis of prostate cancer.
  • To explore the potential of AFAP1-AS1 as a therapeutic target for prostate cancer.

Main Methods:

  • Quantitative real-time PCR (RT-qPCR) to assess AFAP1-AS1 and miR-512-3p expression in prostate cancer tissues and cell lines.
  • Cell proliferation, migration, and invasion assays (e.g., CCK-8, flow cytometry) were performed.
  • Luciferase reporter assays and Western blotting were used to identify downstream targets and protein expression (CDK4, CDK6, CCND1).

Main Results:

  • AFAP1-AS1 was found to be highly expressed in prostate cancer tissues and cell lines, correlating with higher histological grade and distant metastasis.
  • High AFAP1-AS1 expression was associated with lower patient survival rates.
  • Silencing AFAP1-AS1 inhibited cell proliferation and migration, inducing G0/G1 phase cell cycle arrest.
  • AFAP1-AS1 was identified as a regulator of miR-512-3p, mediating its effects on prostate cancer cell progression.

Conclusions:

  • AFAP1-AS1 promotes prostate cancer progression by regulating miR-512-3p, impacting cell proliferation, invasion, and migration.
  • These findings suggest AFAP1-AS1 as a potential therapeutic strategy for prostate cancer treatment.

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