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10.1101/gad.256693.114 http://scihub22266oqcxt.onion/10.1101/gad.256693.114 C4441054!4441054 !25956904     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25956904 &cmd=llinks): Failed to open stream: HTTP request failed! 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LIN28 cooperates with WNT signaling to drive invasive intestinal and colorectal adenocarcinoma in mice and humans |pdf=|usr=}}{{25956904 }} gab.com Text LIN28 cooperates with WNT signaling to drive invasive intestinal and colorectal adenocarcinoma in mice and humans JO: Genes Dev http://www.kidney.de/pget.php?&tw=1&pmid=25956904 #FOAvip Colorectal cancer (CRC) remains a major contributor to cancer-related mortality. LIN28A and LIN28B are highly related RNA-binding protein paralogs that regulate biogenesis of let-7 microRNAs and influence development, metabolism, tissue regeneration, and oncogenesis. Here we demonstrate that overexpression of either LIN28 paralog cooperates with the Wnt pathway to promote invasive intestinal adenocarcinoma in murine models. When LIN28 alone is induced genetically, half of the resulting tumors harbor Ctnnb1 (?-catenin) mutation. When overexpressed in Apc(Min/+) mice, LIN28 accelerates tumor formation and enhances proliferation and invasiveness. In conditional genetic models, enforced expression of a LIN28-resistant form of the let-7 microRNA reduces LIN28-induced tumor burden, while silencing of LIN28 expression reduces tumor volume and increases tumor differentiation, indicating that LIN28 contributes to tumor maintenance. We detected aberrant expression of LIN28A and/or LIN28B in 38% of a large series of human CRC samples (n = 595), where LIN28 expression levels were associated with invasive tumor growth. Our late-stage CRC murine models and analysis of primary human tumors demonstrate prominent roles for both LIN28 paralogs in promoting CRC growth and progression and implicate the LIN28/let-7 pathway as a therapeutic target. Twit Text FOAVip LIN28 cooperates with WNT signaling to drive invasive intestinal and colorectal adenocarcinoma in mice and humans ????Genes Dev http://www.kidney.de/pget.php?&tw=1&pmid=25956904 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25956904 #FOAvip English Wikipedia <ref>{{Cite pmid|25956904 }}</ref> LIN28 cooperates with WNT signaling to drive invasive intestinal and colorectal adenocarcinoma in mice and humans #MMPMID25956904 Tu HC ; Schwitalla S ; Qian Z ; LaPier GS ; Yermalovich A ; Ku YC ; Chen SC ; Viswanathan SR ; Zhu H ; Nishihara R ; Inamura K ; Kim SA ; Morikawa T ; Mima K ; Sukawa Y ; Yang J ; Meredith G ; Fuchs CS ; Ogino S ; Daley GQ Genes Dev 2015[May]; 29 (10 ): 1074-86 PMID25956904 show ga Colorectal cancer (CRC) remains a major contributor to cancer-related mortality. LIN28A and LIN28B are highly related RNA-binding protein paralogs that regulate biogenesis of let-7 microRNAs and influence development, metabolism, tissue regeneration, and oncogenesis. Here we demonstrate that overexpression of either LIN28 paralog cooperates with the Wnt pathway to promote invasive intestinal adenocarcinoma in murine models. When LIN28 alone is induced genetically, half of the resulting tumors harbor Ctnnb1 (?-catenin) mutation. When overexpressed in Apc(Min/+) mice, LIN28 accelerates tumor formation and enhances proliferation and invasiveness. In conditional genetic models, enforced expression of a LIN28-resistant form of the let-7 microRNA reduces LIN28-induced tumor burden, while silencing of LIN28 expression reduces tumor volume and increases tumor differentiation, indicating that LIN28 contributes to tumor maintenance. We detected aberrant expression of LIN28A and/or LIN28B in 38% of a large series of human CRC samples (n = 595), where LIN28 expression levels were associated with invasive tumor growth. Our late-stage CRC murine models and analysis of primary human tumors demonstrate prominent roles for both LIN28 paralogs in promoting CRC growth and progression and implicate the LIN28/let-7 pathway as a therapeutic target. |*Signal Transduction [MESH] |Adenocarcinoma/*physiopathology [MESH] |Animals [MESH] |Colorectal Neoplasms/*physiopathology [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Humans [MESH] |Mice [MESH] |Neoplasm Invasiveness/genetics/physiopathology [MESH] |RNA-Binding Proteins/genetics/*metabolism [MESH]LIN28 cooperates with WNT signaling to drive invasive intestinal and c(epmc).pdf DeepDyve Pubget Overpricing