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Regulation of hormonal therapy resistance by cell cycle machinery

Binoj Chandrasekharan Nair1, Ratna K Vadlamudi

  • 1Department of Obstetrics and Gynecology, The University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229.

Gene Therapy & Molecular Biology
|September 28, 2011
PubMed

Insights

Estrogen Receptor (ER) positive breast cancer can become resistant to hormonal therapy. This review explores how cell cycle machinery contributes to this resistance and identifies potential new therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • Estrogen Receptor (ER) is crucial in ER-positive breast cancer development and progression.
  • Hormonal therapy improves survival but acquired resistance is common.
  • Growth factor signaling pathways and their cross-talk with ER are implicated in resistance.

Purpose of the Study:

  • To review mechanisms of cell cycle machinery in hormonal therapy resistance.
  • To explore cell cycle components as novel therapeutic targets.

Main Methods:

  • Literature review of studies on ER, growth factor signaling, and cell cycle machinery.
  • Analysis of cross-talk between these pathways in therapy resistance.

Main Results:

  • Cell cycle machinery acts as a downstream effector for growth factor signaling in therapy resistance.
  • Deregulation of cell cycle regulators and their cross-talk with ER is observed in resistant tumors.

Conclusions:

  • Understanding cell cycle machinery's role is key to overcoming hormonal therapy resistance.
  • Targeting cell cycle components offers a promising strategy for resistant ER-positive breast cancer.

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