Genomic and Non-Genomic Molecular Basis of Sex Steroid Action in Cancer Cells |
Paper ID : 1148-IGA |
Authors |
Atefeh Hasanli * Department of Nanobiotechnology, Faculty of Biological Science, Tarbiat Modares University, Tehran, Iran |
Abstract |
Background and Aim: 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. Experimental in vitro and in vivo studies focusing on the mechanism of sex steroid action in cancer cells were included. Results: 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 α 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. Further research is required to reveal the exact mechanism of sex steroids on cancer cells. |
Keywords |
Carotenoids, Breast cancer, Antioxidants, Cancer prevention |
Status: Accepted |