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10.1177/1533033818784411 http://scihub22266oqcxt.onion/10.1177/1533033818784411 C6048655!6048655!29986635     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Technol+Cancer+Res+Treat 2018 ; 17 (ä): ä Nephropedia Template TP {{tp|p=29986635|t=2018. Silencing of ENO1 by shRNA Inhibits the Proliferation of Gastric Cancer Cells |pdf=|usr=}}{{29986635}} gab.com Text Silencing of ENO1 by shRNA Inhibits the Proliferation of Gastric Cancer Cells JO: Technol Cancer Res Treat http://www.kidney.de/pget.php?&tw=1&pmid=29986635 #FOAvip ?-Enolase is a significant subunit of enolase and acts as a glycolytic enzyme responsible for catalyzing the conversion of 2-phosphoglycerate to phosphoenolpyruvate in the anaerobic glycolysis pathway. The research about their role is known little in tumor invasion and metastasis. This research analyzed the effect of ?-enolase in proliferation and progression of human gastric cancer. The constructed PLKO.1-ENO1 shRNA vector was transfected into 293 T cells and used to infect gastric cancer cells, MKN45, by using lentivirus method. Negative controls were generated by infection with viruses containing empty vector PLKO.1-scramble-shRNA by the same protocol and using wild-type MKN45 cells as blank control. The silencing effect was confirmed by reverse transcription polymerase chain reaction and Western blotting at messenger RNA and protein levels, respectively. Cell proliferation and chemosensitivity were tested by methyl-thiazolyl-tetrazolium assay. Cell apoptosis was tested by flow cytometry. The cell line ?-enolase short hairpin RNA stabling silence ?-enolase was successfully constructed. In the ?-enolase short hairpin RNA cell lines, messenger RNA and protein expression of ?-enolase were significantly lower than those in negative control and blank control groups. The proliferation and clone formation ability were significantly inhibited, cell apoptosis was increased significantly, and the inhibition rate of chemotherapy drugs was increased (P < .05). Our data provide strong evidence that ?-enolase short hairpin RNA interference vector can effectively suppress the proliferation and increase chemosensitivity of MKN45 cells, which may provide a novel gene therapy for gastric cancer. Twit Text FOAVip Silencing of ENO1 by shRNA Inhibits the Proliferation of Gastric Cancer Cells ????Technol Cancer Res Treat http://www.kidney.de/pget.php?&tw=1&pmid=29986635 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29986635 #FOAvip English Wikipedia <ref>{{Cite pmid|29986635}}</ref> Silencing of ENO1 by shRNA Inhibits the Proliferation of Gastric Cancer Cells #MMPMID29986635 Qiao H; Wang YF; Yuan WZ; Zhu BD; Jiang L; Guan QL Technol Cancer Res Treat 2018[]; 17 (ä): ä PMID29986635show ga ?-Enolase is a significant subunit of enolase and acts as a glycolytic enzyme responsible for catalyzing the conversion of 2-phosphoglycerate to phosphoenolpyruvate in the anaerobic glycolysis pathway. The research about their role is known little in tumor invasion and metastasis. This research analyzed the effect of ?-enolase in proliferation and progression of human gastric cancer. The constructed PLKO.1-ENO1 shRNA vector was transfected into 293 T cells and used to infect gastric cancer cells, MKN45, by using lentivirus method. Negative controls were generated by infection with viruses containing empty vector PLKO.1-scramble-shRNA by the same protocol and using wild-type MKN45 cells as blank control. The silencing effect was confirmed by reverse transcription polymerase chain reaction and Western blotting at messenger RNA and protein levels, respectively. Cell proliferation and chemosensitivity were tested by methyl-thiazolyl-tetrazolium assay. Cell apoptosis was tested by flow cytometry. The cell line ?-enolase short hairpin RNA stabling silence ?-enolase was successfully constructed. In the ?-enolase short hairpin RNA cell lines, messenger RNA and protein expression of ?-enolase were significantly lower than those in negative control and blank control groups. The proliferation and clone formation ability were significantly inhibited, cell apoptosis was increased significantly, and the inhibition rate of chemotherapy drugs was increased (P < .05). Our data provide strong evidence that ?-enolase short hairpin RNA interference vector can effectively suppress the proliferation and increase chemosensitivity of MKN45 cells, which may provide a novel gene therapy for gastric cancer. äSilencing of ENO1 by shRNA Inhibits the Proliferation of Gastric Cance(epmc).pdf DeepDyve Pubget Overpricing