Long Noncoding RNA lncARSR Promotes Doxorubicin Resistance in Hepatocellular Carcinoma via Modulating PTEN-PI3K/Akt

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Yaling Li1, Yun Ye1, Bimin Feng1

  • 1Department of Pharmacy, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.

Journal of Cellular Biochemistry
|May 3, 2017
PubMed

Insights

Long noncoding RNA lncARSR promotes resistance to doxorubicin chemotherapy in hepatocellular carcinoma (HCC). This molecule targets PTEN, activating the PI3K/Akt pathway, and serves as a prognostic biomarker for HCC chemo-resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Hepatocellular carcinoma (HCC) exhibits significant resistance to chemotherapy.
  • The role of long noncoding RNAs (lncRNAs) in HCC chemo-resistance remains largely unexplored.
  • Understanding resistance mechanisms is crucial for improving HCC treatment outcomes.

Purpose of the Study:

  • To investigate the role of lncARSR in mediating chemo-resistance in hepatocellular carcinoma.
  • To elucidate the molecular mechanisms by which lncARSR affects HCC chemo-resistance.
  • To evaluate lncARSR as a potential prognostic biomarker and therapeutic target for HCC.

Main Methods:

  • Quantitative real-time PCR to assess lncARSR and PTEN expression.
  • In vitro and in vivo functional assays (overexpression and knockdown) to evaluate doxorubicin resistance.
  • RNA immunoprecipitation and Western blotting to confirm lncARSR-PTEN interaction and pathway activation.
  • Analysis of clinical HCC tissues for correlation between lncARSR, PTEN, and prognosis.

Main Results:

  • lncARSR is upregulated in HCC tissues and correlates with poor prognosis, larger tumor size, and advanced BCLC stage.
  • Overexpression of lncARSR confers doxorubicin resistance in HCC cells, while its knockdown increases sensitivity.
  • lncARSR promotes PTEN mRNA degradation, leading to decreased PTEN expression and activation of the PI3K/Akt pathway.
  • PTEN expression is negatively correlated with lncARSR levels in HCC tissues.
  • Reversal of chemo-resistance effects by PI3K/Akt pathway inhibitors and PTEN depletion confirmed the mechanism.

Conclusions:

  • Upregulated lncARSR promotes doxorubicin resistance in hepatocellular carcinoma by modulating the PTEN-PI3K/Akt pathway.
  • lncARSR represents a potential prognostic biomarker for HCC.
  • lncARSR may serve as a novel therapeutic target to overcome chemo-resistance in HCC.
Keywords:
DOXORUBICIN CHEMORESISTANCEHEPATOCELLULAR CARCINOMALONG NONCODING RNAPTEN-PI3 K/Akt PATHWAYlncARSR

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