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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.
Abstract:
Recent studies have reported that the long non-coding RNA (lncRNA) AFAP antisense RNA 1 (AFAP1-AS1) is involved in various biological processes and plays a key role in regulating cancer growth and metastasis in humans. However, its effects on tumorigenesis in pituitary adenomas remain unclear. The present study investigated the expression and biological role of AFAP1-AS1 in pituitary adenomas. We observed that the expression of AFAP1-AS1 was considerably higher in the pituitary adenoma tissues as compared to its expression in the adjacent tissues. Additionally, knockdown of AFAP1-AS1 inhibited the proliferation, arrested the cell cycle in the G1-to-S transition phase, and promoted apoptosis in GH3 and MMQ cells. Finally, knockdown of AFAP1-AS1 also promoted the expression of PTEN and inhibited the expression of PI3K and p-AKT. Our results provided novel insights into the function and mechanism of action of AFAP1-AS1 in the pathogenesis of pituitary adenomas.
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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