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10.18632/oncotarget.13343 http://scihub22266oqcxt.onion/10.18632/oncotarget.13343 C5349899!5349899 !27863384     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27863384 &cmd=llinks): Failed to open stream: HTTP request failed! 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A novel highly potent trivalent TGF-? receptor trap inhibits early-stage tumorigenesis and tumor cell invasion in murine Pten-deficient prostate glands |pdf=|usr=}}{{27863384 }} gab.com Text A novel highly potent trivalent TGF- receptor trap inhibits early-stage tumorigenesis and tumor cell invasion in murine Pten-deficient prostate glands JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27863384 #FOAvip The effects of transforming growth factor beta (TGF-?) signaling on prostate tumorigenesis has been shown to be strongly dependent on the stage of development, with TGF-? functioning as a tumor suppressor in early stages of disease and as a promoter in later stages. To study in further detail the paradoxical tumor-suppressive and tumor-promoting roles of the TGF-? pathway, we investigated the effect of systemic treatment with a TGF-? inhibitor on early stages of prostate tumorigenesis. To ensure effective inhibition, we developed and employed a novel trivalent TGF-? receptor trap, RER, comprised of domains derived from the TGF-? type II and type III receptors. This trap was shown to completely block T?RII binding, to antagonize TGF-?1 and TGF-?3 signaling in cultured epithelial cells at low picomolar concentrations, and it showed equal or better anti-TGF-? activities than a pan TGF-? neutralizing antibody and a TGF-? receptor I kinase inhibitor in various prostate cancer cell lines. Systemic administration of RER inhibited prostate tumor cell proliferation as indicated by reduced Ki67 positive cells and invasion potential of tumor cells in high grade prostatic intraepithelial neoplasia (PIN) lesions in the prostate glands of Pten conditional null mice. These results provide evidence that TGF-? acts as a promoter rather than a suppressor in the relatively early stages of this spontaneous prostate tumorigenesis model. Thus, inhibition of TGF-? signaling in early stages of prostate cancer may be a novel therapeutic strategy to inhibit the progression as well as the metastatic potential in patients with prostate cancer. Twit Text FOAVip A novel highly potent trivalent TGF- receptor trap inhibits early-stage tumorigenesis and tumor cell invasion in murine Pten-deficient prostate glands ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27863384 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27863384 #FOAvip English Wikipedia <ref>{{Cite pmid|27863384 }}</ref> A novel highly potent trivalent TGF-? receptor trap inhibits early-stage tumorigenesis and tumor cell invasion in murine Pten-deficient prostate glands #MMPMID27863384 Qin T ; Barron L ; Xia L ; Huang H ; Villarreal MM ; Zwaagstra J ; Collins C ; Yang J ; Zwieb C ; Kodali R ; Hinck CS ; Kim SK ; Reddick RL ; Shu C ; O'Connor-McCourt MD ; Hinck AP ; Sun LZ Oncotarget 2016[Dec]; 7 (52 ): 86087-86102 PMID27863384 show ga The effects of transforming growth factor beta (TGF-?) signaling on prostate tumorigenesis has been shown to be strongly dependent on the stage of development, with TGF-? functioning as a tumor suppressor in early stages of disease and as a promoter in later stages. To study in further detail the paradoxical tumor-suppressive and tumor-promoting roles of the TGF-? pathway, we investigated the effect of systemic treatment with a TGF-? inhibitor on early stages of prostate tumorigenesis. To ensure effective inhibition, we developed and employed a novel trivalent TGF-? receptor trap, RER, comprised of domains derived from the TGF-? type II and type III receptors. This trap was shown to completely block T?RII binding, to antagonize TGF-?1 and TGF-?3 signaling in cultured epithelial cells at low picomolar concentrations, and it showed equal or better anti-TGF-? activities than a pan TGF-? neutralizing antibody and a TGF-? receptor I kinase inhibitor in various prostate cancer cell lines. Systemic administration of RER inhibited prostate tumor cell proliferation as indicated by reduced Ki67 positive cells and invasion potential of tumor cells in high grade prostatic intraepithelial neoplasia (PIN) lesions in the prostate glands of Pten conditional null mice. These results provide evidence that TGF-? acts as a promoter rather than a suppressor in the relatively early stages of this spontaneous prostate tumorigenesis model. Thus, inhibition of TGF-? signaling in early stages of prostate cancer may be a novel therapeutic strategy to inhibit the progression as well as the metastatic potential in patients with prostate cancer. |Animals [MESH] |Carcinogenesis [MESH] |Cell Line, Tumor [MESH] |Cell Proliferation [MESH] |Humans [MESH] |Male [MESH] |Mice [MESH] |Neoplasm Invasiveness [MESH] |Neoplasm Staging [MESH] |PTEN Phosphohydrolase/*physiology [MESH] |Phosphorylation [MESH] |Prostate/*pathology [MESH] |Prostatic Neoplasms/pathology/*prevention & control [MESH] |Proto-Oncogene Proteins c-akt/physiology [MESH] |Receptors, Transforming Growth Factor beta/*antagonists & inhibitors [MESH] |Signal Transduction/physiology [MESH]A novel highly potent trivalent TGF-? receptor trap inhibits early-sta(epmc).pdf DeepDyve Pubget Overpricing