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10.1038/s41419-017-0243-9 http://scihub22266oqcxt.onion/10.1038/s41419-017-0243-9 C5833396!5833396 !29440633     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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29440633 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cell+Death+Dis 2018 ; 9 (2 ): 219 Nephropedia Template TP {{tp|p=29440633 |t=2018. KRAS induces lung tumorigenesis through microRNAs modulation |pdf=|usr=}}{{29440633 }} gab.com Text KRAS induces lung tumorigenesis through microRNAs modulation JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29440633 #FOAvip Oncogenic KRAS induces tumor onset and development by modulating gene expression via different molecular mechanisms. MicroRNAs (miRNAs) are small non-coding RNAs that have been established as main players in tumorigenesis. By overexpressing wild type or mutant KRAS (KRAS(G12D)) and using inducible human and mouse cell lines, we analyzed KRAS-regulated microRNAs in non-small-cell lung cancer (NSCLC). We show that miR-30c and miR-21 are significantly upregulated by both KRAS isoforms and induce drug resistance and enhance cell migration/invasion via inhibiting crucial tumor suppressor genes, such as NF1, RASA1, BID, and RASSF8. MiR-30c and miR-21 levels were significantly elevated in tumors from patients that underwent surgical resection of early stages NSCLC compared to normal lung and in plasma from the same patients. Systemic delivery of LNA-anti-miR-21 in combination with cisplatin in vivo completely suppressed the development of lung tumors in a mouse model of lung cancer. Mechanistically, we demonstrated that ELK1 is responsible for miR-30c and miR-21 transcriptional activation by direct binding to the miRNA proximal promoter regions. In summary, our study defines that miR-30c and miR-21 may be valid biomarkers for early NSCLC detection and their silencing could be beneficial for therapeutic applications. Twit Text FOAVip KRAS induces lung tumorigenesis through microRNAs modulation ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29440633 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29440633 #FOAvip English Wikipedia <ref>{{Cite pmid|29440633 }}</ref> KRAS induces lung tumorigenesis through microRNAs modulation #MMPMID29440633 Shi L ; Middleton J ; Jeon YJ ; Magee P ; Veneziano D ; Laganą A ; Leong HS ; Sahoo S ; Fassan M ; Booton R ; Shah R ; Crosbie PAJ ; Garofalo M Cell Death Dis 2018[Feb]; 9 (2 ): 219 PMID29440633 show ga Oncogenic KRAS induces tumor onset and development by modulating gene expression via different molecular mechanisms. MicroRNAs (miRNAs) are small non-coding RNAs that have been established as main players in tumorigenesis. By overexpressing wild type or mutant KRAS (KRAS(G12D)) and using inducible human and mouse cell lines, we analyzed KRAS-regulated microRNAs in non-small-cell lung cancer (NSCLC). We show that miR-30c and miR-21 are significantly upregulated by both KRAS isoforms and induce drug resistance and enhance cell migration/invasion via inhibiting crucial tumor suppressor genes, such as NF1, RASA1, BID, and RASSF8. MiR-30c and miR-21 levels were significantly elevated in tumors from patients that underwent surgical resection of early stages NSCLC compared to normal lung and in plasma from the same patients. Systemic delivery of LNA-anti-miR-21 in combination with cisplatin in vivo completely suppressed the development of lung tumors in a mouse model of lung cancer. Mechanistically, we demonstrated that ELK1 is responsible for miR-30c and miR-21 transcriptional activation by direct binding to the miRNA proximal promoter regions. In summary, our study defines that miR-30c and miR-21 may be valid biomarkers for early NSCLC detection and their silencing could be beneficial for therapeutic applications. |Animals [MESH] |Carcinogenesis/*genetics [MESH] |Humans [MESH] |Lung Neoplasms/*genetics/physiopathology [MESH] |Mice [MESH] |MicroRNAs/*adverse effects [MESH]KRAS induces lung tumorigenesis through microRNAs modulation (epmc).pdf DeepDyve Pubget Overpricing