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.

10.1002/ijc.30604 http://scihub22266oqcxt.onion/10.1002/ijc.30604 C5324539!5324539!28073170     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       Int+J+Cancer 2017 ; 140 (8): 1881-7 Nephropedia Template TP {{tp|p=28073170|t=2017. Loss of hSef promotes metastasis through upregulation of EMT in prostate cancer |pdf=|usr=}}{{28073170}} gab.com Text Loss of hSef promotes metastasis through upregulation of EMT in prostate cancer JO: Int J Cancer http://www.kidney.de/pget.php?&tw=1&pmid=28073170 #FOAvip We have previously reported that the negative signaling regulator Similar Expression to FGF (hSef) is downregulated in prostate cancer and its loss is associated with clinical metastasis. Here, we explored the mechanistic basis of this finding. We first confirmed our clinical observation by testing hSef manipulation in an in vivo metastasis model. hSef stable expressing cells (PC3M?hSef) or empty vector controls (PC3M?EV) were injected subcutaneously into the lateral thoracic walls of NOD?SCID gamma mice and lungs were harvested at autopsy. In this model, 6/7 PC3M?EV xenografts had definitive lung micro?metastasis whilst only 1/6 PC3M?hSef xenografts exhibited metastasis recapitulating the clinical scenario (p?=?0.03). Gene expression studies revealed key perturbations in genes involved in cell motility and epithelial to mesenchymal transition (EMT) along with alterations in cognate signaling pathways. These results were validated in an EMT specific PCR array whereby hSef over?expression and silencing reciprocally altered E?Cadherin expression (p?=?<0.001) amongst other EMT markers. Immunohistochemistry of excised tumors from the xenografts also confirmed the effect of hSef in suppressing E?Cadherin expression at the protein level. Phosphokinase arrays further demonstrated a role for hSef in attenuating signaling of not only ERK?MAPK but also the JNK and p38 pathways as well. Taken together, these data suggest evidence that loss of hSef may be a critical event facilitating tumor dissemination of prostate cancer through alteration of EMT. Detection of downregulated hSef, along with other negative regulators, may therefore be a useful biomarker heralding a transition to a metastatic phenotype and warrants further exploration in this context. Twit Text FOAVip Loss of hSef promotes metastasis through upregulation of EMT in prostate cancer ????Int J Cancer http://www.kidney.de/pget.php?&tw=1&pmid=28073170 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28073170 #FOAvip English Wikipedia <ref>{{Cite pmid|28073170}}</ref> Loss of hSef promotes metastasis through upregulation of EMT in prostate cancer #MMPMID28073170 Hori S; Wadhwa K; Pisupati V; Zecchini V; Ramos?Montoya A; Warren AY; Neal DE; Gnanapragasam VJ Int J Cancer 2017[Apr]; 140 (8): 1881-7 PMID28073170show ga We have previously reported that the negative signaling regulator Similar Expression to FGF (hSef) is downregulated in prostate cancer and its loss is associated with clinical metastasis. Here, we explored the mechanistic basis of this finding. We first confirmed our clinical observation by testing hSef manipulation in an in vivo metastasis model. hSef stable expressing cells (PC3M?hSef) or empty vector controls (PC3M?EV) were injected subcutaneously into the lateral thoracic walls of NOD?SCID gamma mice and lungs were harvested at autopsy. In this model, 6/7 PC3M?EV xenografts had definitive lung micro?metastasis whilst only 1/6 PC3M?hSef xenografts exhibited metastasis recapitulating the clinical scenario (p?=?0.03). Gene expression studies revealed key perturbations in genes involved in cell motility and epithelial to mesenchymal transition (EMT) along with alterations in cognate signaling pathways. These results were validated in an EMT specific PCR array whereby hSef over?expression and silencing reciprocally altered E?Cadherin expression (p?=?<0.001) amongst other EMT markers. Immunohistochemistry of excised tumors from the xenografts also confirmed the effect of hSef in suppressing E?Cadherin expression at the protein level. Phosphokinase arrays further demonstrated a role for hSef in attenuating signaling of not only ERK?MAPK but also the JNK and p38 pathways as well. Taken together, these data suggest evidence that loss of hSef may be a critical event facilitating tumor dissemination of prostate cancer through alteration of EMT. Detection of downregulated hSef, along with other negative regulators, may therefore be a useful biomarker heralding a transition to a metastatic phenotype and warrants further exploration in this context. äLoss of hSef promotes metastasis through upregulation of EMT in prosta(epmc).pdf DeepDyve Pubget Overpricing