Elevated survivin mediated multidrug resistance and reduced apoptosis in breast cancer stem cells

Chan-Juan Yu1, Jiang-Hua Ou, Ming-Long Wang

  • 1Department of Anesthesia, Xinjiang Medical University Affiliated Tumor Hospital, the Xinjiang Uygur Autonomous Region 830011, China.

Abstract

Insights

Prodigiosin effectively targets survivin in breast cancer stem cells, inducing apoptosis and overcoming drug resistance. This highlights survivin

Area of Science:

  • Cancer Biology
  • Molecular Oncology
  • Pharmacology

Background:

  • Survivin overexpression in breast cancer drives uncontrolled cell proliferation by inhibiting apoptosis.
  • Breast cancer stem-like side population (SP) cells exhibit enhanced survival mechanisms.
  • SP cells are implicated in multidrug resistance and therapeutic failure.

Purpose of the Study:

  • To investigate the role of survivin in breast cancer stem-like SP cells.
  • To evaluate the efficacy of prodigiosin in downregulating survivin and inducing apoptosis in these cells.
  • To assess the impact of prodigiosin on drug resistance and chemosensitivity of SP cells.

Main Methods:

  • Quantification of survivin expression levels in breast cancer SP cells.
  • Assessment of apoptosis rates, drug resistance, and colony formation post-prodigiosin treatment.
  • Analysis of stem cell marker expression (Oct-4, EpCAM, ABCG2) in SP cells.

Main Results:

  • Breast cancer samples showed approximately 2.7% SP cells with elevated stem cell marker expression.
  • SP cells overexpressed survivin, correlating with reduced apoptosis and increased multidrug resistance.
  • Prodigiosin treatment sensitized SP cells to apoptosis and conventional chemotherapeutic agents.

Conclusions:

  • Increased survivin expression in breast cancer SP cells is a key factor in apoptosis evasion and chemotherapy resistance.
  • Targeting survivin with agents like prodigiosin offers a potential strategy to enhance breast cancer treatment efficacy.
  • Prodigiosin demonstrates promise in overcoming drug resistance mediated by survivin in cancer stem cells.

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