By Gabriella Castoria, Antimo Migliaccio
Breast and prostate cancers are either hormone-dependent, at the very least in a few phases in their development. Hormonal manipulation represents an immense healing procedure. even if such a lot of breast and prostate cancers at the beginning reply to hormone remedy, such a lot tumors reinitiate to development. ultimately, hormone-resistant and metastatic breast and prostate cancers may possibly improve. therefore, the problem is the dissection of mechanisms wherein steroid receptor signaling pathways proceed to steer phone progress and invasiveness. Compelling proof exhibits that steroid hormones elicit non-genomic responses in extra-nuclear compartment of aim cells. during this mobile place, steroid-coupled receptors quickly recruit signaling effectors or scaffold proteins and turn on a number of pathways resulting in proliferation, survival, migration and invasiveness. The instant problem is the dissection of key occasions regulating the steroid reaction of goal tissues to avoid development and increase therapy 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
J. edu J. E. Pritchard Department of Microbiology, University of Virginia Cancer Center, Charlottesville, VA 22908, USA E. M. Fox Hematology/Oncology Division, Ingram Cancer Center, Vanderbilt University, Nashville, TN 37240, USA M. A. Shupnik Department of Medicine, Division of Endocrinology, University of Virginia Cancer Center, Charlottesville, VA 22908, USA G. Castoria and A. 1007/978-1-4614-1764-4_3, Ó Springer Science+Business Media, LLC 2012 31 32 S. J. Parsons et al. e. ER or PR) heregulin insulin-like growth factor-1 ligand-binding domain modulator of non-genomic action of estrogen receptor Matrix metallo-proteinase non-small cell lung cancer PI3-kinase progesterone receptor serine Src family kinase Src homology 3 steroid coactivator-1 transforming growth factor tyrosine kinase inhibitor tyrosine Contents 1 2 3 Introduction..........................................................................................................................
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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