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Induction of paclitaxel resistance by ERα mediated prohibitin mitochondrial-nuclear shuttling

Pei Dong1, Lijuan Jiang2, Jianye Liu2

  • 1State Key Laboratory of Oncology in South China, Department of Urology, Sun Yat-sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, Guangzhou, Guangdong, China ; Guangdong Key Laboratory of Urology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.

Plos One
|December 31, 2013
PubMed

Insights

Estrogen (E2) treatment induces Paclitaxel resistance in prostate cancer cells by activating estrogen receptor alpha (ERα), which promotes Prohibitin (PHB) translocation and suppresses proliferation. PHB mediates this estrogen-dependent resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • Paclitaxel is a key anticancer agent, but its efficacy is limited by cellular resistance.
  • Estrogen signaling pathways are implicated in various cancers, including prostate cancer.
  • Understanding mechanisms of drug resistance is crucial for improving cancer therapy.

Purpose of the Study:

  • To investigate the role of estrogen in mediating Paclitaxel resistance in prostate cancer cells.
  • To elucidate the molecular mechanisms underlying estrogen-induced Paclitaxel resistance.
  • To identify potential therapeutic targets for overcoming Paclitaxel resistance.

Main Methods:

  • Modeling Paclitaxel resistance in vitro using estrogen-treated PC-3 and LNCaP prostate cancer cells.
  • Utilizing small interfering RNA (siRNA) to knockdown estrogen receptor alpha (ERα).
  • Analyzing the effects of estrogen (E2), ERα, and Prohibitin (PHB) on cellular proliferation and Paclitaxel sensitivity.

Main Results:

  • Estrogen (E2) treatment induced Paclitaxel resistance in androgen-independent PC-3 cells, but not in LNCaP cells.
  • Knockdown of ERα decreased E2-induced Paclitaxel resistance in androgen-independent cells.
  • E2 promoted Prohibitin (PHB) mitochondrial-nucleus translocation via ERα, inhibiting cellular proliferation and mediating Paclitaxel resistance.
  • PHB was identified downstream of ERα, mediating estrogen-dependent Paclitaxel resistance signaling.

Conclusions:

  • Estrogen receptor alpha (ERα) plays a critical role in mediating estrogen-dependent Paclitaxel resistance in prostate cancer.
  • Prohibitin (PHB) acts downstream of ERα and is essential for the development of Paclitaxel resistance.
  • Targeting the ERα-PHB signaling pathway may offer a strategy to overcome Paclitaxel resistance in prostate cancer.

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