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.

10.3892/ol.2016.5305 http://scihub22266oqcxt.onion/10.3892/ol.2016.5305 C5103973!5103973!27900025     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncol+Lett 2016 ; 12 (5): 3485-91 Nephropedia Template TP {{tp|p=27900025|t=2016. PBX3 promotes gastric cancer invasion and metastasis by inducing epithelial-mesenchymal transition |pdf=|usr=}}{{27900025}} gab.com Text PBX3 promotes gastric cancer invasion and metastasis by inducing epithelial-mesenchymal transition JO: Oncol Lett http://www.kidney.de/pget.php?&tw=1&pmid=27900025 #FOAvip The overexpression of pre-leukemia transcription factor 3 (PBX3) in tumors plays an important role in invasion, metastasis and proliferation in a variety of human cancer types. Tumor metastasis and angiogenesis significantly contribute to the progression of cancer and create challenges for cancer therapy. In the present study, reverse transcription-polymerase chain reaction demonstrated that PBX3 was upregulated in gastric cancer (GC) tissues and Transwell assay revealed that the overexpression of PBX3 promoted GC invasion and metastasis in vitro. In addition, a nude mouse xenograft model was established, which demonstrated that PBX3 promoted peritoneal metastases in vivo. Furthermore, the overexpression of PBX3 in GC promoted the tubular formation of human umbilical vein endothelial cells. Western blot analysis revealed that overexpressed PBX3 induced epithelial-mesenchymal transition (EMT) in GC, as measured by increases in the EMT protein markers N-cadherin and vimentin, while E-cadherin expression was reduced in PBX3-overexpressing GC cells. Contrasting results were observed in PBX3-knockdown GC cells. Additionally, the overexpression of PBX3 increased the levels of phosphorylated AKT (Ser473), which is involved in the progression of a variety of human cancers. Gelatin zymography assay demonstrated that the overexpression of PBX3 also elevated matrix metalloproteinase-9 activity in GC, which was closely associated with tumor metastasis and angiogenesis. Based on these findings, it may be concluded that PBX3 enhances invasion and metastasis in GC by promoting EMT, possibly via the AKT signaling pathway. Twit Text FOAVip PBX3 promotes gastric cancer invasion and metastasis by inducing epithelial-mesenchymal transition ????Oncol Lett http://www.kidney.de/pget.php?&tw=1&pmid=27900025 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27900025 #FOAvip English Wikipedia <ref>{{Cite pmid|27900025}}</ref> PBX3 promotes gastric cancer invasion and metastasis by inducing epithelial-mesenchymal transition #MMPMID27900025 Wang S; Li C; Wang W; Xing C Oncol Lett 2016[Nov]; 12 (5): 3485-91 PMID27900025show ga The overexpression of pre-leukemia transcription factor 3 (PBX3) in tumors plays an important role in invasion, metastasis and proliferation in a variety of human cancer types. Tumor metastasis and angiogenesis significantly contribute to the progression of cancer and create challenges for cancer therapy. In the present study, reverse transcription-polymerase chain reaction demonstrated that PBX3 was upregulated in gastric cancer (GC) tissues and Transwell assay revealed that the overexpression of PBX3 promoted GC invasion and metastasis in vitro. In addition, a nude mouse xenograft model was established, which demonstrated that PBX3 promoted peritoneal metastases in vivo. Furthermore, the overexpression of PBX3 in GC promoted the tubular formation of human umbilical vein endothelial cells. Western blot analysis revealed that overexpressed PBX3 induced epithelial-mesenchymal transition (EMT) in GC, as measured by increases in the EMT protein markers N-cadherin and vimentin, while E-cadherin expression was reduced in PBX3-overexpressing GC cells. Contrasting results were observed in PBX3-knockdown GC cells. Additionally, the overexpression of PBX3 increased the levels of phosphorylated AKT (Ser473), which is involved in the progression of a variety of human cancers. Gelatin zymography assay demonstrated that the overexpression of PBX3 also elevated matrix metalloproteinase-9 activity in GC, which was closely associated with tumor metastasis and angiogenesis. Based on these findings, it may be concluded that PBX3 enhances invasion and metastasis in GC by promoting EMT, possibly via the AKT signaling pathway. äPBX3 promotes gastric cancer invasion and metastasis by inducing epith(epmc).pdf DeepDyve Pubget Overpricing