MiR-92a-3p Promotes the Malignant Progression of Hepatocellular Carcinoma by Mediating the PI3K/AKT/mTOR Signaling Pathway

Curr Pharm Des. 2021;27(29):3244-3250. doi: 10.2174/1381612827666210612054156.

Abstract

Background: As one of the most common cancers globally, hepatocellular carcinoma (HCC) usually has a poor prognosis. Many HCC patients are usually diagnosed at advanced stages. Therefore, new potential biomarkers for the diagnosis and prognosis of HCC are urgently needed. More and more studies have shown that miR-92a-3p can regulate the occurrence and development of various cancers, but its clinical significance and molecular mechanism in HCC are still elusive. Here, we tried to clarify the regulatory mechanism of miR-92a-3p in HCC.

Methods: In this study, we conducted qRT-PCR and revealed that miR-92a-3p was notably upregulated in HCC cells. MTT, flow cytometry, wound healing, Transwell invasion assays and western blot were conducted to uncover that overexpressed miR-92a-3p could boost the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of HCC cells while inhibiting cell apoptosis. In addition, the proteins associated with the PI3K/AKT/mTOR pathway were also detected by western blot.

Results: It was suggested that miR-92a-3p could activate the PI3K/AKT/mTOR signaling pathway.

Conclusion: These results suggest that miR-92a-3p plays a tumor-promoting role in HCC and may be a potential biomarker for the diagnosis and prognosis of HCC.

Keywords: Hepatocellular carcinoma (HCC); MTT; MiRNAs.; PI3K/AKT/mTOR signaling pathway; epithelial-mesenchymal transition (EMT); miR-92a-3p.

MeSH terms

  • Carcinoma, Hepatocellular* / genetics
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Liver Neoplasms* / genetics
  • MicroRNAs* / genetics
  • Phosphatidylinositol 3-Kinases / genetics
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction
  • TOR Serine-Threonine Kinases / genetics

Substances

  • MIRN92 microRNA, human
  • MicroRNAs
  • MTOR protein, human
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases