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Long non-coding RNA SNHG1 protects human AC16 cardiomyocytes from doxorubicin toxicity by regulating miR-195/Bcl-2

Sisi Chen1,2,3, Jichun Wang4,2,3, Yanli Zhou4,2,3

  • 1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China chensisi6617@163.com.

Bioscience Reports
|July 14, 2019
PubMed

Insights

Long non-coding RNA SNHG1 protects heart cells from Doxorubicin toxicity by regulating the miR-195/Bcl-2 pathway. This finding offers potential therapeutic strategies for mitigating chemotherapy-induced heart damage.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Oncology

Background:

  • Doxorubicin (DOX) is a potent anti-cancer drug.
  • DOX-induced cardiotoxicity limits its clinical use.
  • The role of long non-coding RNAs (lncRNAs) in DOX cardiotoxicity is under investigation.

Purpose of the Study:

  • To investigate the regulatory role of lncRNA SNHG1 in Doxorubicin toxicity in AC16 cardiomyocytes.
  • To elucidate the molecular mechanisms underlying SNHG1's effect on DOX-induced cardiotoxicity.

Main Methods:

  • AC16 cardiomyocytes were treated with Doxorubicin (DOX).
  • Expression levels of SNHG1 and miR-195 were analyzed.
  • Cell viability and apoptosis were assessed.
  • The interaction between SNHG1, miR-195, and Bcl-2 was investigated.

Main Results:

  • DOX treatment decreased AC16 cell viability and increased apoptosis.
  • DOX reduced SNHG1 expression in AC16 cells.
  • Overexpression of SNHG1 attenuated DOX-induced apoptosis.
  • SNHG1 counteracted miR-195's inhibition of Bcl-2; miR-195 restoration abolished SNHG1's protective effect.

Conclusions:

  • SNHG1 protects human AC16 cardiomyocytes against Doxorubicin toxicity.
  • This protection is partly mediated by the regulation of the miR-195/Bcl-2 axis.
  • SNHG1 represents a potential therapeutic target for managing DOX cardiotoxicity.
Keywords:
apoptosiscardiotoxicitydoxorubicinlong non-coding RNA SNHG1miR-195

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