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Salinomycin triggers endoplasmic reticulum stress through ATP2A3 upregulation in PC-3 cells

Yunsheng Zhang1, Fang Li2, Luogen Liu3

  • 1Clinical Research Institute, The Second Affiliated Hospital, University of South China; Clinical Research Center For Breast & Thyroid Disease Prevention In Hunan Province, Hengyang, 421001, People's Republic of China.

BMC Cancer
|April 27, 2019
PubMed
Abstract

Insights

Salinomycin, a potential chemotherapy drug, targets prostate cancer by upregulating ATP2A3, inhibiting calcium release, and inducing endoplasmic reticulum stress, leading to cancer cell apoptosis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Salinomycin is a potential chemotherapy agent with demonstrated efficacy against prostate cancer stem cells.
  • The precise molecular mechanisms underlying salinomycin's anti-cancer effects remain largely unelucidated.
  • Identifying salinomycin's molecular targets is crucial for its therapeutic development.

Purpose of the Study:

  • To identify the molecular targets of salinomycin in prostate cancer.
  • To investigate the role of ATP2A3 in salinomycin's anti-cancer activity.
  • To elucidate the involvement of endoplasmic reticulum (ER) stress in salinomycin's mechanism of action.

Main Methods:

  • Gene expression microarray analysis was performed on PC-3 cells and a xenograft model treated with salinomycin.
  • Western blotting and immunohistochemistry were used to assess ATP2A3 and ER stress biomarker expression.
  • Flow cytometry analyzed cell cycle, apoptosis, and intracellular calcium (Ca2+) levels.

Main Results:

  • Salinomycin treatment significantly upregulated ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 3 (ATP2A3).
  • ATP2A3 overexpression induced ER stress and exhibited anti-cancer effects in prostate cancer cell lines.
  • Salinomycin-induced ER stress, potentially mediated by ATP2A3-linked Ca2+ release, promoted apoptosis in prostate cancer cells.

Conclusions:

  • ATP2A3 is identified as a potential molecular target of salinomycin in prostate cancer.
  • Salinomycin exerts anti-cancer effects by inhibiting Ca2+ release and inducing ER stress via ATP2A3.
  • This study provides mechanistic insights into salinomycin's therapeutic potential for prostate cancer.
Keywords:
ATP2A3ApoptosisCa2+ releaseER stressSalinomycin

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