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MicroRNA-216b is downregulated in hepatocellular carcinoma and inhibits HepG2 cell growth by targeting Forkhead box

W-W Zheng1, J Zhou, C-H Zhang

  • 1Department of Gastroenterology, Weifang Traditional Chinese Hospital, Weifang City, Shandong Province, China. zww554478@163.com.

European Review for Medical and Pharmacological Sciences
|July 8, 2016
PubMed
Abstract

Insights

Decreased microRNA-216b (miR-216b) expression in hepatocellular carcinoma (HCC) promotes tumor growth by upregulating FOXM1. Restoring miR-216b levels may offer a potential therapeutic strategy for HCC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Aberrant microRNA (miRNA) expression is implicated in cancer development.
  • MicroRNAs play crucial roles in regulating cellular processes, including tumorigenesis.
  • Hepatocellular carcinoma (HCC) is a significant global health concern with complex molecular underpinnings.

Purpose of the Study:

  • To investigate the expression profile of miR-216b in hepatocellular carcinoma (HCC).
  • To elucidate the functional role of miR-216b in HCC cell proliferation, cell cycle, and apoptosis.
  • To identify the molecular mechanism underlying miR-216b's function, specifically its interaction with FOXM1.

Main Methods:

  • Quantitative Real-time PCR (qRT-PCR) to assess miR-216b and FOXM1 expression in HCC tissues.
  • In vitro assays including MTT for proliferation, flow cytometry for cell cycle analysis, and ELISA for apoptosis.
  • Western blot analysis for cleaved-caspase-3 and luciferase reporter assays to validate direct targeting of FOXM1 by miR-216b.

Main Results:

  • miR-216b was significantly downregulated, while FOXM1 was upregulated in HCC tissues, showing an inverse correlation.
  • Overexpression of miR-216b suppressed HepG2 cell proliferation, induced cell cycle arrest, and promoted apoptosis.
  • miR-216b was confirmed to directly target the 3' UTR of FOXM1, leading to decreased FOXM1 expression.

Conclusions:

  • Downregulation of miR-216b contributes to hepatocellular carcinoma (HCC) tumorigenicity by increasing FOXM1 levels.
  • The miR-216b/FOXM1 axis represents a critical regulatory pathway in HCC.
  • miR-216b holds potential as a therapeutic target or agent for HCC treatment.

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