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LncRNA FGD5-AS1 functions as an oncogene to upregulate GTPBP4 expression by sponging miR-873-5p in hepatocellular

Nuobei Zhang1, Hao Shen2, Shenan Huang3

  • 1Department of Gastroenterology, The Second Affiliated Hospital of Nanchang University, Nanchang. znbicx@163.com.

European Journal of Histochemistry : EJH
|November 16, 2021
PubMed

Insights

Long non-coding FGD5-AS1 (LncFGD5-AS1) promotes hepatocellular carcinoma (HCC) progression by sponging miR-873-5p, affecting GTP-binding protein 4 (GTPBP4). This reveals a potential therapeutic target for HCC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer.
  • The specific function of FGD5-AS1 in hepatocellular carcinoma (HCC) remains largely uncharacterized.
  • LncRNAs can regulate tumor progression by interacting with microRNAs (miRNAs).

Purpose of the Study:

  • To investigate the expression pattern and biological role of FGD5-AS1 in HCC.
  • To elucidate the molecular mechanism underlying FGD5-AS1's function in HCC progression.
  • To identify potential therapeutic targets for HCC based on FGD5-AS1 regulation.

Main Methods:

  • Quantitative real-time PCR (RT-qPCR) for expression analysis.
  • Cellular assays including CCK-8, EdU, flow cytometry, wound healing, and Transwell assays to assess proliferation, apoptosis, migration, and invasion.
  • Dual-luciferase reporter and RNA pull-down assays to determine molecular interactions.

Main Results:

  • FGD5-AS1 expression was significantly upregulated in HCC tissues and cell lines.
  • Knockdown of FGD5-AS1 inhibited HCC cell proliferation, migration, and invasion, while inducing apoptosis.
  • FGD5-AS1 acts as a competing endogenous RNA by sponging miR-873-5p, and regulates GTP-binding protein 4 (GTPBP4) expression via the miR-873-5p/GTPBP4 axis.

Conclusions:

  • FGD5-AS1 plays a crucial oncogenic role in HCC progression.
  • The miR-873-5p/GTPBP4 axis is identified as a direct downstream pathway regulated by FGD5-AS1.
  • Targeting the FGD5-AS1/miR-873-5p/GTPBP4 pathway offers a promising therapeutic strategy for HCC.

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