By Gabriella Castoria, Antimo Migliaccio
Breast and prostate cancers are either hormone-dependent, at the very least in a few levels in their development. Hormonal manipulation represents an enormous healing method. even supposing such a lot of breast and prostate cancers at the beginning reply to hormone remedy, so much tumors reinitiate to development. ultimately, hormone-resistant and metastatic breast and prostate cancers might improve. therefore, the problem is the dissection of mechanisms in which steroid receptor signaling pathways proceed to steer telephone development and invasiveness. Compelling proof exhibits that steroid hormones elicit non-genomic responses in extra-nuclear compartment of objective 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 aim 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
C-Src has been implicated in colorectal, breast, melanoma, ovarian, gastric, head and neck, pancreatic, lung, brain, and blood cancer development/progression , though it is poorly oncogenic on its own. However, mice expressing endogenous c-Src and the polyomavirus middle T antigen transgene under the control of a mammary-specific promoter form more tumors at a faster rate than those expressing polyomavirus middle T on a c-Src null background , indicating that c-Src can cooperate with other oncogenic factors to enhance tumorigenicity.
Estrogen-induced ER association with Shc stimulates c-Src-mediated ERK activation. 4. Estrogen increases ER and c-Src association with MNAR and c-Src activation, resulting in ERK phosphorylation and increased transcription from ERE-containing promoters. 5. Estrogen induces the formation of an ER, p130Cas, and c-Src complex, which supports ERK phosphorylation and cyclin D1 expression. 6. The association of AR and c-Src activate ERK through an estrogen and ER-dependent mechanism. 7. Type IV collagen signals through integrins, ER, and c-Src to induce transcription from ERE-containing promoters.
Several small-molecule inhibitors and monoclonal antibodies are currently being tested or used in the clinic for the treatment of these tumors. Keywords Estrogen receptor Á Progesterone receptor Á Androgen receptor Á c-Src Á HER family receptors Á Therapeutic resistance S. 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.