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Long Noncoding RNA SOX2-OT Aggravates Doxorubicin-Induced Apoptosis of Cardiomyocyte by Targeting miR-942-5p/DP5

Haining Wang1, Xiule Lin1, Jilin Li2

  • 1Department of Cardiovascular Medicine, The First Affiliated Hospital of Shantou University Medical College, Cardiac Care Unit (CCU), Shantou, Guangdong Province, 515041, People's Republic of China.

Drug Design, Development and Therapy
|February 19, 2021
PubMed
Abstract

Insights

Long non-coding RNA SOX2-OT promotes doxorubicin-induced cardiomyocyte apoptosis by upregulating DP5 via sponging miR-942-5p. Knockdown of SOX2-OT protects cardiomyocytes from doxorubicin-induced apoptosis.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • RNA Biology

Background:

  • Long non-coding RNAs (LncRNAs) are implicated in doxorubicin (DOX)-induced cardiomyocyte apoptosis.
  • The specific role of lncRNA SOX2-OT in this process remains largely unknown.

Purpose of the Study:

  • To investigate the function of SOX2-OT in doxorubicin-induced cardiomyocyte apoptosis.
  • To elucidate the molecular mechanism involving SOX2-OT, miR-942-5p, and DP5.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) and immunoblotting to assess expression levels.
  • Luciferase reporter assays to determine molecular interactions.
  • Annexin V-FITC/PI staining, caspase-3 activity assays, and TUNEL staining to evaluate apoptosis.
  • Echocardiography for in vivo assessment.

Main Results:

  • SOX2-OT and DP5 expression were elevated, while miR-942-5p was decreased in DOX-treated cardiomyocytes and a rat model.
  • SOX2-OT acts as a sponge for miR-942-5p, directly targeting it and upregulating DP5.
  • miR-942-5p counteracted the protective effects of SOX2-OT knockdown by inhibiting DP5 expression.

Conclusions:

  • Knockdown of SOX2-OT inhibits doxorubicin-induced cardiomyocyte apoptosis.
  • This protective effect is mediated by downregulating DP5 through sponging miR-942-5p.
Keywords:
DP5apoptosiscardiomyocytelncRNA SOX2-OTmiR-942-5p

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