Knockdown of long non-coding RNA AFAP1-AS1 inhibits growth and promotes apoptosis in pituitary adenomas

Hengxin Tang1, Bo Hou1, Zhuopeng Ye1

  • 1Department of Neurosurgery, Third Affiliated Hospital, Sun Yat-sen University Guangzhou, Guangdong, China.

Insights

The long non-coding RNA AFAP1-AS1 is highly expressed in pituitary tumors. Reducing its levels inhibits tumor cell growth and promotes cell death, offering new therapeutic targets.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • Long non-coding RNAs (lncRNAs) regulate gene expression and are implicated in various cancers.
  • The role of AFAP antisense RNA 1 (AFAP1-AS1) in pituitary adenoma tumorigenesis is not well understood.

Purpose of the Study:

  • To investigate the expression and biological function of AFAP1-AS1 in pituitary adenomas.
  • To elucidate the molecular mechanism underlying AFAP1-AS1's role in pituitary adenoma development.

Main Methods:

  • Quantitative real-time PCR to assess AFAP1-AS1 expression in pituitary adenoma tissues and adjacent normal tissues.
  • In vitro experiments involving knockdown of AFAP1-AS1 in pituitary adenoma cell lines (GH3 and MMQ).
  • Cell proliferation assays, cell cycle analysis, apoptosis assays, and Western blotting to analyze downstream signaling pathways (PTEN, PI3K, p-AKT).

Main Results:

  • AFAP1-AS1 expression was significantly upregulated in pituitary adenoma tissues compared to adjacent tissues.
  • Knockdown of AFAP1-AS1 suppressed proliferation, induced G1-to-S cell cycle arrest, and promoted apoptosis in pituitary adenoma cells.
  • AFAP1-AS1 knockdown led to increased PTEN expression and decreased PI3K/p-AKT signaling.

Conclusions:

  • AFAP1-AS1 plays a crucial role in the pathogenesis of pituitary adenomas.
  • Targeting AFAP1-AS1 may represent a potential therapeutic strategy for pituitary adenomas by modulating the PTEN/PI3K/AKT pathway.

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