Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1007/s10549-017-4211-y http://scihub22266oqcxt.onion/10.1007/s10549-017-4211-y C5427117!5427117 !28337662     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28337662 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Breast+Cancer+Res+Treat 2017 ; 163 (3 ): 449-460 Nephropedia Template TP {{tp|p=28337662 |t=2017. A83-01 inhibits TGF-?-induced upregulation of Wnt3 and epithelial to mesenchymal transition in HER2-overexpressing breast cancer cells |pdf=|usr=}}{{28337662 }} gab.com Text A83-01 inhibits TGF- -induced upregulation of Wnt3 and epithelial to mesenchymal transition in HER2-overexpressing breast cancer cells JO: Breast Cancer Res Treat http://www.kidney.de/pget.php?&tw=1&pmid=28337662 #FOAvip PURPOSE: The aim of this study is to investigate the mechanisms of interactions between TGF-? and Wnt/?-catenin pathways that induce and regulate EMT and promote breast cancer cells to become resistant to treatment. METHODS: The effect of TGF-? on Wnt/?-catenin signaling pathway was examined by using a human Wnt/?-catenin-regulated cDNA plate array and western blot analysis. The interaction of Twist at promoter of Wnt3 was examined by chromatin immunoprecipitation (ChIP) assay. Secreted Wnt3 level was determined by ELISA assay. RESULTS: HER2-overexpressing breast cancer cells treated with TGF-? have a reduced response to trastuzumab and exhibited EMT-like phenotype. The TGF-?-induced EMT in HER2-cells was concordant with upregulation of Wnt3 and ?-catenin pathways. The TGF-?-induced induction of Wnt3 during EMT was found to be Smad3-dependent. ChIP analysis identified occupancy of Twist at promoter region of Wnt3. Knock-down of Twist by shRNA confirmed the significance of Twist in response to TGF-? regulating Wnt3 during EMT. Subsequently, TGF-?-induced matrix metalloproteinases, MMP1, MMP7, MMP9, MMP26, Vascular endothelial growth factors (VEGF), and activation of Wnt/?-catenin signaling were repressed by the shRNA treatment. TGF-?R1 ALK5 kinase inhibitor, A83-01 can effectively prevent the TGF-?-induced Twist and Wnt3. Co-treating A83-01 and trastuzumab inhibited TGF-?-induced cell invasion significantly in both trastuzumab responsive and resistant cells. CONCLUSIONS: Our data demonstrated an important interdependence between TGF-? and Wnt/?-catenin pathways inducing EMT in HER2-overexpressing breast cancer cells. Twist served as a linkage between the two pathways during TGF-?-induced EMT. A83-01 could inhibit the TGF-?-initiated pathway interactions and enhance HER2-cells response to trastuzumab treatment. Twit Text FOAVip A83-01 inhibits TGF- -induced upregulation of Wnt3 and epithelial to mesenchymal transition in HER2-overexpressing breast cancer cells ????Breast Cancer Res Treat http://www.kidney.de/pget.php?&tw=1&pmid=28337662 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28337662 #FOAvip English Wikipedia <ref>{{Cite pmid|28337662 }}</ref> A83-01 inhibits TGF-?-induced upregulation of Wnt3 and epithelial to mesenchymal transition in HER2-overexpressing breast cancer cells #MMPMID28337662 Wu Y ; Tran T ; Dwabe S ; Sarkissyan M ; Kim J ; Nava M ; Clayton S ; Pietras R ; Farias-Eisner R ; Vadgama JV Breast Cancer Res Treat 2017[Jun]; 163 (3 ): 449-460 PMID28337662 show ga PURPOSE: The aim of this study is to investigate the mechanisms of interactions between TGF-? and Wnt/?-catenin pathways that induce and regulate EMT and promote breast cancer cells to become resistant to treatment. METHODS: The effect of TGF-? on Wnt/?-catenin signaling pathway was examined by using a human Wnt/?-catenin-regulated cDNA plate array and western blot analysis. The interaction of Twist at promoter of Wnt3 was examined by chromatin immunoprecipitation (ChIP) assay. Secreted Wnt3 level was determined by ELISA assay. RESULTS: HER2-overexpressing breast cancer cells treated with TGF-? have a reduced response to trastuzumab and exhibited EMT-like phenotype. The TGF-?-induced EMT in HER2-cells was concordant with upregulation of Wnt3 and ?-catenin pathways. The TGF-?-induced induction of Wnt3 during EMT was found to be Smad3-dependent. ChIP analysis identified occupancy of Twist at promoter region of Wnt3. Knock-down of Twist by shRNA confirmed the significance of Twist in response to TGF-? regulating Wnt3 during EMT. Subsequently, TGF-?-induced matrix metalloproteinases, MMP1, MMP7, MMP9, MMP26, Vascular endothelial growth factors (VEGF), and activation of Wnt/?-catenin signaling were repressed by the shRNA treatment. TGF-?R1 ALK5 kinase inhibitor, A83-01 can effectively prevent the TGF-?-induced Twist and Wnt3. Co-treating A83-01 and trastuzumab inhibited TGF-?-induced cell invasion significantly in both trastuzumab responsive and resistant cells. CONCLUSIONS: Our data demonstrated an important interdependence between TGF-? and Wnt/?-catenin pathways inducing EMT in HER2-overexpressing breast cancer cells. Twist served as a linkage between the two pathways during TGF-?-induced EMT. A83-01 could inhibit the TGF-?-initiated pathway interactions and enhance HER2-cells response to trastuzumab treatment. |Breast Neoplasms/*drug therapy/genetics/pathology [MESH] |Cell Line, Tumor [MESH] |Drug Resistance, Neoplasm/genetics [MESH] |Epithelial-Mesenchymal Transition/genetics [MESH] |Female [MESH] |Gene Expression Regulation, Neoplastic/drug effects [MESH] |Humans [MESH] |Protein Serine-Threonine Kinases/antagonists & inhibitors/genetics [MESH] |Pyrazoles/administration & dosage [MESH] |Receptor, ErbB-2/*genetics [MESH] |Receptor, Transforming Growth Factor-beta Type I [MESH] |Receptors, Transforming Growth Factor beta/antagonists & inhibitors/genetics [MESH] |Thiosemicarbazones/administration & dosage [MESH] |Transforming Growth Factor beta/*genetics [MESH] |Trastuzumab/administration & dosage [MESH] |Twist-Related Protein 1/genetics [MESH] |Vascular Endothelial Growth Factor A/genetics [MESH] |Wnt Signaling Pathway/drug effects [MESH] |Wnt3 Protein/*genetics [MESH]A83-01 inhibits TGF-?-induced upregulation of Wnt3 and epithelial to m(epmc).pdf DeepDyve Pubget Overpricing