Molecular Pathways of Genomic and Non-Genomic Sex Steroid Effects in Cancer Cells
Paper ID : 1156-IGA
Authors
Afrooz Sepahvand *
Department of Cellular and Molecular Biology, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
Abstract
Although association of sex steroids, including estrogens
androgens, and progestogens, with cancer cells proliferation, differentiation, and
apoptosis has been reported in many studies, the precise mechanism of sex steroids
action in cancer cells remains to be revealed. This study aims to explore the molecular
mechanisms by which sex steroids influence cancer cells growth and proliferation.
Method: A review of the literature was conducted using databases such as PubMed,
Scopus, and Web of Science, covering studies published between 2000 and 2024.
xperimental in vitro and in vivo studies focusing on the mechanism of sex steroid action
in cancer cells were included.
kesults: Anticancer effects of estrogen, progesterone and testosterone can be mediated
through both genomic and non-genomic pathways. In breast cancer cells, p130Cas has
been shown to interact with estrogen receptor a and modulate non-genomic estrogen
signaling. Recent evidence also suggests a cross-talk between tyrosine phosphorylation
signaling and steroid hormone action in epithelial cells, including prostate and breast
cancer cells. Shc adaptor proteins, specifically p52(Shc) and p66(Shc), have been
implicated in mediating steroid hormone-regulated cancers through a novel molecular
mechanism involving redox signaling induced by p66(Shc). Sex steroids can induce
intrinsic and extrinsic apoptotic pathways in cancer cells
Conclusion: Sex steroids influence cancer cells growth, proliferation and differentiations
through genomic and non-genomic pathways and may have carcinogenic or anticancer
effects in human tissues, urther research is required to reveal the exact mechanism of
sex steroids on cancer cells.
Keywords
Sex steroids, Genomic, Non-Genomic, Molecular mechanism
Status: Accepted