Targeting rapid action of sex-steroid receptors in breast and prostate cancers.

Human breast and prostate cancers are complex diseases caused by the progressive accumulation of gene mutations combined with epigenetic deregulation of critical genes and derangement of signaling pathways. Compelling evidence indicates that steroid hormones elicit non-genomic responses in cytoplasm of target cells. In this cellular location, steroid-coupled receptors recruit signaling effectors or scaffold proteins, thereafter activating multiple pathways leading to proliferation, survival, migration and invasiveness.

Targeting rapid action of sex steroid receptors in breast and prostate cancers.

Human breast and prostate cancers are complex diseases caused by the progressive accumulation of gene mutations combined with epigenetic deregulation of critical genes and derangement of signaling pathways. Compelling evidence indicates that steroid hormones elicit non-genomic responses in cytoplasm of target cells. In this cellular location, steroid-coupled receptors recruit signaling effectors or scaffold proteins, thereafter activating multiple pathways leading to proliferation, survival, migration and invasiveness.

Androgen-induced cell migration: role of androgen receptor/filamin A association.

Background: Androgen receptor (AR) controls male morphogenesis, gametogenesis and prostate growth as well as development of prostate cancer. These findings support a role for AR in cell migration and invasiveness. However, the molecular mechanism involved in AR-mediated cell migration still remains elusive.

Steroid signaling activation and intracellular localization of sex steroid receptors.

In addition to stimulating gene transcription, sex steroids trigger rapid, non-genomic responses in the extra-nuclear compartment of target cells. These events take place within seconds or minutes after hormone administration and do not require transcriptional activity of sex steroid receptors. Depending on cell systems, activation of extra-nuclear signaling pathways by sex steroids fosters cell cycle progression, prevents apoptosis, leads to epigenetic modifications and increases cell migration through cytoskeleton changes.