Non-genomic androgen action regulates proliferative/migratory signaling in stromal cells

Front Endocrinol (Lausanne). 2015 Jan 19:5:225. doi: 10.3389/fendo.2014.00225. eCollection 2014.

Abstract

Prostate cancer (PCa) is the major cause of cancer-related death among the male population of Western society, and androgen-deprivation therapy (ADT) represents the first line in PCa treatment. However, although androgen receptor (AR) expression is maintained throughout the various stages of PCa, ADT frequently fails. Clinical studies have demonstrated that different androgen/AR signaling pathways operate in target tissues. AR stimulates growth and transformation of target cells, but under certain conditions slows down their proliferation. In this review, we discuss the role of AR in controlling different functions of mesenchymal and transformed mesenchymal cells. Findings here presented support the role of AR in suppressing proliferation and stimulating migration of stromal cells, with implications for current approaches to cancer therapy.

Keywords: androgen receptor; fibroblasts; fibrosarcoma; filamin A; growth suppression; migration.

Publication types

  • Review