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10.18632/oncotarget.4305 http://scihub22266oqcxt.onion/10.18632/oncotarget.4305 C4662463!4662463 !26056085     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26056085 &cmd=llinks): Failed to open stream: HTTP request failed! 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Underexpression of LKB1 tumor suppressor is associated with enhanced Wnt signaling and malignant characteristics of human intrahepatic cholangiocarcinoma |pdf=|usr=}}{{26056085 }} gab.com Text Underexpression of LKB1 tumor suppressor is associated with enhanced Wnt signaling and malignant characteristics of human intrahepatic cholangiocarcinoma JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26056085 #FOAvip Intrahepatic cholangiocarcinoma (ICC) is a rare and highly aggressive malignancy. In this study, we identified the presence of gene deletion and missense mutation leading to inactivation or underexpression of liver kinase B1 (LKB1) tumor suppressor and excluded the involvement of LKB1 gene hypermethylation in ICC tissues. Immunohistochemical analysis showed that LKB1 was underexpressed in a portion of 326 ICC tissues compared to their adjacent normal tissues. By statistical analysis underexpression of LKB1 in ICC tissues significantly correlated with poor survival and malignant disease characteristics in ICC patients. Moreover, we showed that knockdown of LKB1 significantly enhanced growth, migration, and invasion of three LKB1-competent ICC cell lines. Global transcriptional profiling analysis identified multiple malignancy-promoting genes, such as HIF-1?, CD24, Talin1, Vinculin, Wnt5, and signaling pathways including Hedgehog, Wnt/?-catenin, and cell adhesion as novel targets of LKB1 underexpression in ICC cells. Furthermore, knockdown of LKB1 gene expression dramatically enhanced Wnt/?-catenin signaling in ICC cells, while an inverse correlation between LKB1 and nuclear ?-catenin was observed in ICC tissues. Our findings suggest a novel mechanism for ICC carcinogenesis in which LKB1 underexpression enhances multiple signaling pathways including Wnt/?-catenin to promote disease progression. Twit Text FOAVip Underexpression of LKB1 tumor suppressor is associated with enhanced Wnt signaling and malignant characteristics of human intrahepatic cholangiocarcinoma ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26056085 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26056085 #FOAvip English Wikipedia <ref>{{Cite pmid|26056085 }}</ref> Underexpression of LKB1 tumor suppressor is associated with enhanced Wnt signaling and malignant characteristics of human intrahepatic cholangiocarcinoma #MMPMID26056085 Wang J ; Zhang K ; Wang J ; Wu X ; Liu X ; Li B ; Zhu Y ; Yu Y ; Cheng Q ; Hu Z ; Guo C ; Hu S ; Mu B ; Tsai CH ; Li J ; Smith L ; Yang L ; Liu Q ; Chu P ; Chang V ; Zhang B ; Wu M ; Jiang X ; Yen Y Oncotarget 2015[Aug]; 6 (22 ): 18905-20 PMID26056085 show ga Intrahepatic cholangiocarcinoma (ICC) is a rare and highly aggressive malignancy. In this study, we identified the presence of gene deletion and missense mutation leading to inactivation or underexpression of liver kinase B1 (LKB1) tumor suppressor and excluded the involvement of LKB1 gene hypermethylation in ICC tissues. Immunohistochemical analysis showed that LKB1 was underexpressed in a portion of 326 ICC tissues compared to their adjacent normal tissues. By statistical analysis underexpression of LKB1 in ICC tissues significantly correlated with poor survival and malignant disease characteristics in ICC patients. Moreover, we showed that knockdown of LKB1 significantly enhanced growth, migration, and invasion of three LKB1-competent ICC cell lines. Global transcriptional profiling analysis identified multiple malignancy-promoting genes, such as HIF-1?, CD24, Talin1, Vinculin, Wnt5, and signaling pathways including Hedgehog, Wnt/?-catenin, and cell adhesion as novel targets of LKB1 underexpression in ICC cells. Furthermore, knockdown of LKB1 gene expression dramatically enhanced Wnt/?-catenin signaling in ICC cells, while an inverse correlation between LKB1 and nuclear ?-catenin was observed in ICC tissues. Our findings suggest a novel mechanism for ICC carcinogenesis in which LKB1 underexpression enhances multiple signaling pathways including Wnt/?-catenin to promote disease progression. |*Wnt Signaling Pathway [MESH] |AMP-Activated Protein Kinase Kinases [MESH] |Base Sequence [MESH] |Bile Duct Neoplasms/enzymology/genetics/*metabolism/*pathology [MESH] |Cell Growth Processes/physiology [MESH] |Cell Line, Tumor [MESH] |Cell Movement/physiology [MESH] |Cholangiocarcinoma/enzymology/genetics/*metabolism/*pathology [MESH] |DNA Methylation [MESH] |Down-Regulation [MESH] |Female [MESH] |Gene Knockdown Techniques [MESH] |Genes, Tumor Suppressor [MESH] |Humans [MESH] |Male [MESH] |Middle Aged [MESH] |Molecular Sequence Data [MESH] |Protein Serine-Threonine Kinases/*biosynthesis/metabolism [MESH]Underexpression of LKB1 tumor suppressor is associated with enhanced W(epmc).pdf DeepDyve Pubget Overpricing