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10.1007/s10555-013-9488-7 http://scihub22266oqcxt.onion/10.1007/s10555-013-9488-7 C4087108!4087108!24398859     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Metastasis+Rev 2014 ; 33 (ä): 497-509 Nephropedia Template TP {{tp|p=24398859|t=2014. RANK-mediated signaling network and cancer metastasis |pdf=|usr=}}{{24398859}} gab.com Text RANK-mediated signaling network and cancer metastasis JO: Cancer Metastasis Rev http://www.kidney.de/pget.php?&tw=1&pmid=24398859 #FOAvip Cancer metastasis is highly inefficient and complex. Common features of metastatic cancer cells have been observed using cancer cell lines and genetically reconstituted mouse and human tumor xenograft models. These include cancer cell interaction with the tumor microenvironment, and the ability of cancer cells to sense extracellular stimuli and adapt to adverse growth conditions. This review summarizes the coordinated response of cancer cells to soluble growth factors, such as RANKL, by a unique forward feedback mechanism employing coordinated upregulation of RANKL and c-Met with downregulation of androgen receptor. The RANK-mediated signal network was found to drive epithelial to mesenchymal transition in prostate cancer cells, promote osteomimicry and the ability of prostate cancer cells to assume stem cell and neuroendocrine phenotypes, and confer the ability of prostate cancer cells to home to bone. Prostate cancer cells with activated RANK-mediated signal network were observed to recruit and even transform the non-tumorigenic prostate cancer cells to participate in bone and soft tissue colonization. The coordinated regulation of cancer cell invasion and metastasis by the forward feedback mechanism involving RANKL, c-Met, transcription factors and VEGF-neuropilin could offer new therapeutic opportunities to target prostate cancer bone and soft tissue metastases. Twit Text FOAVip RANK-mediated signaling network and cancer metastasis ????Cancer Metastasis Rev http://www.kidney.de/pget.php?&tw=1&pmid=24398859 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24398859 #FOAvip English Wikipedia <ref>{{Cite pmid|24398859}}</ref> RANK-mediated signaling network and cancer metastasis #MMPMID24398859 Chu CYG; Chung LWK Cancer Metastasis Rev 2014[Sep]; 33 (ä): 497-509 PMID24398859show ga Cancer metastasis is highly inefficient and complex. Common features of metastatic cancer cells have been observed using cancer cell lines and genetically reconstituted mouse and human tumor xenograft models. These include cancer cell interaction with the tumor microenvironment, and the ability of cancer cells to sense extracellular stimuli and adapt to adverse growth conditions. This review summarizes the coordinated response of cancer cells to soluble growth factors, such as RANKL, by a unique forward feedback mechanism employing coordinated upregulation of RANKL and c-Met with downregulation of androgen receptor. The RANK-mediated signal network was found to drive epithelial to mesenchymal transition in prostate cancer cells, promote osteomimicry and the ability of prostate cancer cells to assume stem cell and neuroendocrine phenotypes, and confer the ability of prostate cancer cells to home to bone. Prostate cancer cells with activated RANK-mediated signal network were observed to recruit and even transform the non-tumorigenic prostate cancer cells to participate in bone and soft tissue colonization. The coordinated regulation of cancer cell invasion and metastasis by the forward feedback mechanism involving RANKL, c-Met, transcription factors and VEGF-neuropilin could offer new therapeutic opportunities to target prostate cancer bone and soft tissue metastases. äRANK-mediated signaling network and cancer metastasis (epmc).pdf DeepDyve Pubget Overpricing