Download Advances in Rapid Sex-Steroid Action: New Challenges and New by Gabriella Castoria, Antimo Migliaccio PDF

By Gabriella Castoria, Antimo Migliaccio

Breast and prostate cancers are either hormone-dependent, not less than in a few levels in their development. Hormonal manipulation represents a major healing procedure. even though such a lot of breast and prostate cancers firstly reply to hormone treatment, so much tumors reinitiate to progress. ultimately, hormone-resistant and metastatic breast and prostate cancers could improve. hence, the problem is the dissection of mechanisms in which steroid receptor signaling pathways proceed to steer telephone progress and invasiveness. Compelling proof shows that steroid hormones elicit non-genomic responses in extra-nuclear compartment of aim cells. during this mobile position, 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 rapid problem is the dissection of key occasions regulating the steroid reaction of objective tissues to avoid development and increase 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

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Gerhardt H, et al. (2003) VEGF guides angiogenic sprouting utilizing endothelial tip cell filopodia. J Cell Biol 161:1163–1177 13. De Donatis A, Comito G, Buricchi F, Vinci MC, Parenti A, Caselli A, Camici G, Manao G, Ramponi G, Cirri P (2008) Proliferation versus migration in platelet-derived growth factor signaling: the key role of endocytosis. J Biol Chem 283:19948–19956 14. Castoria G, Lombardi M, Barone MV, Bilancio A, Di Domenico M, Bottero D, Vitale F, Migliaccio A, Auricchio F (2003) Androgen stimulated DNA synthesis and cytoskeletal changes in fibroblasts by a non transcriptional receptor action.

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The 12 A. Migliaccio et al. molecular basis of ER and AR associations with Src triggered by either steroid hormones or EGF has been discussed in previous sections of this chapter together with their role in hormone- or growth factor-dependent growth. ER alpha or ER beta association with Src occurs in mammary cancer and prostate cancer cells, respectively. This association can be suppressed by nanomolar concentration of a small peptide mimicking the sequence surrounding ER alpha phosphotyrosine 537, which interacts with Src-SH2 domain [47].

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