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Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer
10:36

Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer

Published on: March 17, 2016

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Pushing estrogen receptor around in breast cancer

Elgene Lim1, Gerard Tarulli2, Neil Portman1

  • 1Garvan Institute of Medical Research and St Vincent's HospitalUniversity of New South Wales, Sydney, New South Wales, Australia.

Endocrine-Related Cancer
|October 13, 2016
PubMed

Insights

Activating progesterone receptor (PR) or androgen receptor (AR) may overcome resistance in estrogen receptor-α (ER)-positive breast cancer. Harnessing these sex steroid receptors (SSRs) can reprogram ER activity towards inhibiting tumor growth.

Area of Science:

  • Oncology
  • Endocrinology
  • Molecular Biology

Background:

  • Estrogen receptor-α (ER) is a key target in ER-positive breast cancer, but treatment resistance remains a significant challenge.
  • Emerging evidence suggests other sex steroid receptors (SSRs) can modulate ER's DNA binding and suppress its oncogenic activity.
  • Progesterone receptor (PR) and androgen receptor (AR) show potential in reprogramming ER towards anti-tumorigenic functions.

Purpose of the Study:

  • To review the clinical evidence for activating PR or AR in ER-positive breast cancer.
  • To explore how PR and AR can inhibit the tumor growth-promoting functions of ER.
  • To highlight the potential of co-targeting ER with other SSRs to overcome treatment resistance.

Main Methods:

  • Review of established and emerging clinical data.
  • Analysis of preclinical and clinical studies investigating PR and AR in breast cancer.
  • Focus on the mechanisms by which PR and AR influence ER DNA binding and gene expression.

Main Results:

  • Activating PR reprograms ER DNA binding towards genes associated with favorable outcomes.
  • AR activation inhibits normal breast and ER-positive tumor growth.
  • Clinical trials are evaluating therapies that leverage SSRs to enhance anti-tumorigenic ER activity.

Conclusions:

  • Targeting PR or AR alongside ER represents a promising strategy to overcome treatment resistance in ER-positive breast cancer.
  • Harnessing the suppressive functions of PR and AR on ER offers a novel therapeutic approach.
  • Further clinical investigation is warranted to optimize combination therapies involving SSRs for breast cancer treatment.
Keywords:
androgen receptorbreast cancerendocrine resistanceendocrine therapyestrogen receptorprogesterone receptor

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