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miR-145 regulates chemoresistance in hepatocellular carcinoma via epithelial mesenchymal transition

B-L Ju1, Y-B Chen1, W-Y Zhang1

  • 1General Hospital of Beijing Command, PLA. Department of Hepatobilliary Surgery Beijing China.

Cellular and Molecular Biology (Noisy-Le-Grand, France)
|June 13, 2015
PubMed

Insights

MicroRNA-145 (miR-145) is reduced in drug-resistant liver cancer (HCC). Increasing miR-145 boosts chemotherapy effectiveness and suppresses cancer cell changes, offering a potential new treatment strategy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Hepatocellular carcinoma (HCC) exhibits significant resistance to chemotherapeutic drugs, hindering effective treatment.
  • MicroRNA-145 (miR-145), a known tumor suppressor, is frequently downregulated in various cancers, including HCC.
  • Adriamycin (ADM) resistance is a critical challenge in HCC therapy, necessitating novel therapeutic approaches.

Purpose of the Study:

  • To investigate the role and therapeutic potential of miR-145 in adriamycin (ADM)-resistant human HCC cells.
  • To determine the effect of miR-145 up-regulation on ADM cytotoxicity and chemoresistance in HCC.
  • To identify the molecular targets of miR-145 and elucidate its mechanism in regulating chemoresistance and epithelial-mesenchymal transition (EMT) in HCC.

Main Methods:

  • Quantitative real-time PCR to assess miR-145 levels in ADM-resistant HCC cell lines (HepG2/ADM, HuH7/ADM) and parental cells.
  • Cell viability assays to evaluate ADM cytotoxicity following miR-145 mimic transfection.
  • Western blotting and luciferase reporter assays to validate Smad3 as a direct target of miR-145.
  • Analysis of EMT markers (E-cadherin, vimentin) to assess miR-145's effect on cellular phenotype.

Main Results:

  • miR-145 expression was significantly lower in ADM-resistant HCC cells compared to sensitive cells.
  • Overexpression of miR-145 enhanced ADM-induced cytotoxicity in chemoresistant HCC cells.
  • Smad3 was confirmed as a direct target of miR-145, with miR-145 inhibiting its expression at both mRNA and protein levels.
  • miR-145 up-regulation suppressed Smad3-mediated EMT, evidenced by increased E-cadherin and decreased vimentin expression.

Conclusions:

  • miR-145 plays a crucial role in modulating chemoresistance and EMT in HCC.
  • Restoring miR-145 levels can overcome ADM resistance in HCC cells by targeting Smad3.
  • Upregulation of miR-145 represents a promising therapeutic strategy for treating chemoresistant HCC.

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