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10.1038/s41419-017-0048-x http://scihub22266oqcxt.onion/10.1038/s41419-017-0048-x C5870598!5870598!29238068     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2017 ; 8 (12): ä Nephropedia Template TP {{tp|p=29238068|t=2017. MicroRNA-105 is involved in TNF-?-related tumor microenvironment enhanced colorectal cancer progression |pdf=|usr=}}{{29238068}} gab.com Text MicroRNA-105 is involved in TNF- -related tumor microenvironment enhanced colorectal cancer progression JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29238068 #FOAvip TNF-? is a central proinflammatory cytokine contributing to malignant tumor progression in tumor microenvironment. In this study, we found the upregulation of miR-105 in colorectal cancer was associated with aggressive phenotype, and the enhanced expression of miR-105 was required for TNF-?-induced epithelial?mesenchymal transition (EMT). The expression of miR-105 was remarkably stimulated by TNF-? in a time-dependent manner using real-time qPCR analysis. Inhibition of miR-105 remarkably weakened the aggressive effects of TNF-? through preventing the activation of NF-?B signaling and the initiation of EMT. Furthermore, miR-105 was demonstrated directly targeted on the 3?-UTRs of RAP2C, a Rap2 subfamily of small GTP-binding protein. Consistently, suppression of RAP2C stimulated the role of miR-105, which dramatically promoted the invasion and metastasis of CRC cells. Thalidomide, a TNF-? and NF-?B inhibitor, significantly weakened the metastasis and homing capacity of miR-105-overexpressed CRC cells in nude mice. Our investigation initiatively illustrated the modulatory role of miR-105 in TNF-?-induced EMT and further CRC metastasis. We also offer a better understanding of TNF?-induced metastasis and suggest an effective therapeutic strategy against CRC metastasis. Twit Text FOAVip MicroRNA-105 is involved in TNF- -related tumor microenvironment enhanced colorectal cancer progression ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29238068 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29238068 #FOAvip English Wikipedia <ref>{{Cite pmid|29238068}}</ref> MicroRNA-105 is involved in TNF-?-related tumor microenvironment enhanced colorectal cancer progression #MMPMID29238068 Shen Z; Zhou R; Liu C; Wang Y; Zhan W; Shao Z; Liu J; Zhang F; Xu L; Zhou X; Qi L; Bo F; Ding Y; Zhao L Cell Death Dis 2017[Dec]; 8 (12): ä PMID29238068show ga TNF-? is a central proinflammatory cytokine contributing to malignant tumor progression in tumor microenvironment. In this study, we found the upregulation of miR-105 in colorectal cancer was associated with aggressive phenotype, and the enhanced expression of miR-105 was required for TNF-?-induced epithelial?mesenchymal transition (EMT). The expression of miR-105 was remarkably stimulated by TNF-? in a time-dependent manner using real-time qPCR analysis. Inhibition of miR-105 remarkably weakened the aggressive effects of TNF-? through preventing the activation of NF-?B signaling and the initiation of EMT. Furthermore, miR-105 was demonstrated directly targeted on the 3?-UTRs of RAP2C, a Rap2 subfamily of small GTP-binding protein. Consistently, suppression of RAP2C stimulated the role of miR-105, which dramatically promoted the invasion and metastasis of CRC cells. Thalidomide, a TNF-? and NF-?B inhibitor, significantly weakened the metastasis and homing capacity of miR-105-overexpressed CRC cells in nude mice. Our investigation initiatively illustrated the modulatory role of miR-105 in TNF-?-induced EMT and further CRC metastasis. We also offer a better understanding of TNF?-induced metastasis and suggest an effective therapeutic strategy against CRC metastasis. äMicroRNA-105 is involved in TNF-?-related tumor microenvironment enhan(epmc).pdf DeepDyve Pubget Overpricing