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10.1002/path.4385 http://scihub22266oqcxt.onion/10.1002/path.4385 C4138305!4138305 !24890125     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24890125 &cmd=llinks): Failed to open stream: HTTP request failed! 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Loss of the novel tumour suppressor and polarity gene Trim62 (Dear1) synergizes with oncogenic Ras in invasive lung cancer |pdf=|usr=}}{{24890125 }} gab.com Text Loss of the novel tumour suppressor and polarity gene Trim62 (Dear1) synergizes with oncogenic Ras in invasive lung cancer JO: J Pathol http://www.kidney.de/pget.php?&tw=1&pmid=24890125 #FOAvip Deregulation of cell polarity proteins has been linked to the processes of invasion and metastasis. TRIM62 is a regulator of cell polarity and a tumour suppressor in breast cancer. Here, we demonstrate that human non-small cell lung cancer lesions show a step-wise loss of TRIM62 levels during disease progression, which was associated with poor clinical outcomes. To directly examine the role of Trim62 in development of lung cancer, we deleted Trim62 in a mutant K-Ras mouse model of lung cancer. In this context, haploinsufficiency of Trim62 synergized with a K-RasG12D mutation to promote invasiveness and disrupt three-dimensional morphogenesis, both of which are associated with epithelial-mesenchymal transitions. Re-expression of Trim62 reverted these phenotypes in tumour cell lines. Thus, Trim62 loss cooperates with K-Ras mutation in tumourigenesis and metastasis in vivo, indicating that decreased levels of TRIM62 may play an important role in the evolution of lung cancer. Twit Text FOAVip Loss of the novel tumour suppressor and polarity gene Trim62 (Dear1) synergizes with oncogenic Ras in invasive lung cancer ????J Pathol http://www.kidney.de/pget.php?&tw=1&pmid=24890125 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24890125 #FOAvip English Wikipedia <ref>{{Cite pmid|24890125 }}</ref> Loss of the novel tumour suppressor and polarity gene Trim62 (Dear1) synergizes with oncogenic Ras in invasive lung cancer #MMPMID24890125 Quintás-Cardama A ; Post SM ; Solis LM ; Xiong S ; Yang P ; Chen N ; Wistuba II ; Killary AM ; Lozano G J Pathol 2014[Sep]; 234 (1 ): 108-19 PMID24890125 show ga Deregulation of cell polarity proteins has been linked to the processes of invasion and metastasis. TRIM62 is a regulator of cell polarity and a tumour suppressor in breast cancer. Here, we demonstrate that human non-small cell lung cancer lesions show a step-wise loss of TRIM62 levels during disease progression, which was associated with poor clinical outcomes. To directly examine the role of Trim62 in development of lung cancer, we deleted Trim62 in a mutant K-Ras mouse model of lung cancer. In this context, haploinsufficiency of Trim62 synergized with a K-RasG12D mutation to promote invasiveness and disrupt three-dimensional morphogenesis, both of which are associated with epithelial-mesenchymal transitions. Re-expression of Trim62 reverted these phenotypes in tumour cell lines. Thus, Trim62 loss cooperates with K-Ras mutation in tumourigenesis and metastasis in vivo, indicating that decreased levels of TRIM62 may play an important role in the evolution of lung cancer. |*Gene Expression Regulation, Neoplastic [MESH] |Animals [MESH] |Carcinoma, Non-Small-Cell Lung/*genetics/pathology [MESH] |Cell Transformation, Neoplastic [MESH] |Epithelial-Mesenchymal Transition [MESH] |Female [MESH] |Genes, ras/*genetics [MESH] |Humans [MESH] |Lung Neoplasms/*genetics/pathology [MESH] |Lung/metabolism/pathology [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Mice, Inbred C57BL [MESH] |Mutation [MESH] |Receptors, Angiotensin/genetics/metabolism [MESH] |Receptors, Endothelin/genetics/metabolism [MESH] |Tripartite Motif Proteins [MESH] |Tumor Suppressor Proteins/*genetics/metabolism [MESH]Loss of the novel tumour suppressor and polarity gene Trim62 (Dear1) s(epmc).pdf DeepDyve Pubget Overpricing