By Gabriella Castoria, Antimo Migliaccio
Breast and prostate cancers are either hormone-dependent, no less than in a few levels in their development. Hormonal manipulation represents an immense healing strategy. even supposing so much of breast and prostate cancers at the beginning reply to hormone remedy, so much tumors reinitiate to progress. eventually, hormone-resistant and metastatic breast and prostate cancers may perhaps boost. therefore, the problem is the dissection of mechanisms wherein steroid receptor signaling pathways proceed to steer mobile development and invasiveness. Compelling facts shows that steroid hormones elicit non-genomic responses in extra-nuclear compartment of goal cells. during this mobile place, steroid-coupled receptors swiftly recruit signaling effectors or scaffold proteins and turn on a number of pathways resulting in proliferation, survival, migration and invasiveness. The speedy problem is the dissection of key occasions regulating the steroid reaction of goal tissues to avoid development and enhance remedy of breast and prostate cancers.
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Extra info for Advances in Rapid Sex-Steroid Action: New Challenges and New Chances in Breast and Prostate Cancers
P. Vicent et al. recruitment of the activated ternary complex of pPR, pERK and pMSK1 to target chromatin, leading to phosphoacetylation of histone H3 and displacement of an HP1~c containing repressive complex. Thus, progestin activation of the Src/Ras/Erk/ Msk1 cascade directly impacts chromatin. Within one minute of adding synthetic progesterone analogues to breast cancer cells, PR recruits to the target genes an ATP-dependent chromatin remodeling complex, NURF, a histone methyltransferase complex, ASCOM, which trimethylates histone H3 at lysine 4, and an activated Cyclin A/CDK2 complex, that phosphorylates histone H1 and facilitates its displacement.
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ITALY). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The authors declare that no competing interests exist. References 1. Pietras RJ, Szego CM (1977) Specific binding sites for oestrogen at the outer surfaces of isolated endometrial cells. Nature 265:69–72 2. Szego CM, Davis JS (1967) Adenosine 30 , 50 -monophosphate in rat uterus: acute elevation by estrogen. Proc Natl Acad Sci USA 58:1711–1718 Non-genomic Action of Steroid Hormones 13 3.