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miR-155-5p antagonizes the apoptotic effect of bufalin in triple-negative breast cancer cells

Qian Wang1, Ce Li, Zhitu Zhu

  • 1aDepartment of Medical Oncology, The First Hospital of China Medical University bDepartment of Urology, The Liaoning Provincial Tumor Hospital, Shenyang cDepartment of Medical Oncology dCancer Research Center, The First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning, People's Republic of China.

Anti-Cancer Drugs
|September 24, 2015
PubMed

Insights

Triple-negative breast cancer (TNBC) cells show reduced sensitivity to bufalin. This study reveals that miR-155-5p upregulation, potentially via DNA methyltransferases 1 and 3a (DNMT1 and DNMT3a) downregulation, contributes to this resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Bufalin, a cardiotonic steroid from toad venom, exhibits anti-tumor properties.
  • Triple-negative breast cancer (TNBC) cells display lower sensitivity to bufalin compared to other breast cancer subtypes.
  • The mechanisms underlying bufalin resistance in TNBC remain largely unknown.

Purpose of the Study:

  • To investigate the role of microRNA-155-5p (miR-155-5p) in bufalin sensitivity in TNBC cells.
  • To elucidate the relationship between bufalin, miR-155-5p, and DNA methyltransferases (DNMTs) in TNBC.

Main Methods:

  • Induction of apoptosis and assessment of miR-155-5p expression in TNBC cell lines (MDA-MB-231, MCF-7/ADR) treated with bufalin.
  • Manipulation of miR-155-5p expression (overexpression and downregulation) to evaluate its impact on bufalin-induced apoptosis and proliferation.
  • Analysis of the effects of bufalin and DNMT inhibition on DNMT1 and DNMT3a expression and their correlation with miR-155-5p levels.

Main Results:

  • Bufalin treatment induced apoptosis in TNBC cells, concurrently increasing miR-155-5p expression.
  • Overexpression of miR-155-5p enhanced TNBC cell proliferation and conferred resistance to bufalin-induced apoptosis.
  • Downregulation of miR-155-5p sensitized TNBC cells to bufalin and increased FOXO3A expression.
  • Bufalin treatment downregulated DNMT1 and DNMT3a, while concurrent inhibition of these enzymes significantly upregulated miR-155-5p expression.

Conclusions:

  • miR-155-5p acts as a negative regulator of bufalin sensitivity in triple-negative breast cancer.
  • Downregulation of DNA methyltransferases 1 and 3a (DNMT1 and DNMT3a) is implicated in the bufalin-induced upregulation of miR-155-5p.
  • Targeting miR-155-5p or modulating DNMT activity may represent potential therapeutic strategies for overcoming bufalin resistance in TNBC.

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