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10.1093/nar/gku860 http://scihub22266oqcxt.onion/10.1093/nar/gku860 C4191424!4191424 !25249619     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25249619 &cmd=llinks): Failed to open stream: HTTP request failed! 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Non-metastatic 2 (NME2)-mediated suppression of lung cancer metastasis involves transcriptional regulation of key cell adhesion factor vinculin |pdf=|usr=}}{{25249619 }} gab.com Text Non-metastatic 2 (NME2)-mediated suppression of lung cancer metastasis involves transcriptional regulation of key cell adhesion factor vinculin JO: Nucleic Acids Res http://www.kidney.de/pget.php?&tw=1&pmid=25249619 #FOAvip Tumor metastasis refers to spread of a tumor from site of its origin to distant organs and causes majority of cancer deaths. Although >30 metastasis suppressor genes (MSGs) that negatively regulate metastasis have been identified so far, two issues are poorly understood: first, which MSGs oppose metastasis in a tumor type, and second, which molecular function of MSG controls metastasis. Herein, integrative analyses of tumor-transcriptomes (n=382), survival data (n=530) and lymph node metastases (n=100) in lung cancer patients identified non-metastatic 2 (NME2) as a key MSG from a pool of >30 metastasis suppressors. Subsequently, we generated a promoter-wide binding map for NME2 using chromatin immunoprecipitation with promoter microarrays (ChIP-chip), and transcriptome profiling. We discovered novel targets of NME2 which are involved in focal adhesion signaling. Importantly, we detected binding of NME2 in promoter of focal adhesion factor, vinculin. Reduced expression of NME2 led to enhanced transcription of vinculin. In comparison, NME1, a close homolog of NME2, did not bind to vinculin promoter nor regulate its expression. In line, enhanced metastasis of NME2-depleted lung cancer cells was found in zebrafish and nude mice tumor models. The metastatic potential of NME2-depleted cells was remarkably diminished upon selective RNA-i-mediated silencing of vinculin. Together, we demonstrate that reduced NME2 levels lead to transcriptional de-repression of vinculin and regulate lung cancer metastasis. Twit Text FOAVip Non-metastatic 2 (NME2)-mediated suppression of lung cancer metastasis involves transcriptional regulation of key cell adhesion factor vinculin ????Nucleic Acids Res http://www.kidney.de/pget.php?&tw=1&pmid=25249619 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25249619 #FOAvip English Wikipedia <ref>{{Cite pmid|25249619 }}</ref> Non-metastatic 2 (NME2)-mediated suppression of lung cancer metastasis involves transcriptional regulation of key cell adhesion factor vinculin #MMPMID25249619 Thakur RK ; Yadav VK ; Kumar A ; Singh A ; Pal K ; Hoeppner L ; Saha D ; Purohit G ; Basundra R ; Kar A ; Halder R ; Kumar P ; Baral A ; Kumar MJ ; Baldi A ; Vincenzi B ; Lorenzon L ; Banerjee R ; Kumar P ; Shridhar V ; Mukhopadhyay D ; Chowdhury S Nucleic Acids Res 2014[Oct]; 42 (18 ): 11589-600 PMID25249619 show ga Tumor metastasis refers to spread of a tumor from site of its origin to distant organs and causes majority of cancer deaths. Although >30 metastasis suppressor genes (MSGs) that negatively regulate metastasis have been identified so far, two issues are poorly understood: first, which MSGs oppose metastasis in a tumor type, and second, which molecular function of MSG controls metastasis. Herein, integrative analyses of tumor-transcriptomes (n=382), survival data (n=530) and lymph node metastases (n=100) in lung cancer patients identified non-metastatic 2 (NME2) as a key MSG from a pool of >30 metastasis suppressors. Subsequently, we generated a promoter-wide binding map for NME2 using chromatin immunoprecipitation with promoter microarrays (ChIP-chip), and transcriptome profiling. We discovered novel targets of NME2 which are involved in focal adhesion signaling. Importantly, we detected binding of NME2 in promoter of focal adhesion factor, vinculin. Reduced expression of NME2 led to enhanced transcription of vinculin. In comparison, NME1, a close homolog of NME2, did not bind to vinculin promoter nor regulate its expression. In line, enhanced metastasis of NME2-depleted lung cancer cells was found in zebrafish and nude mice tumor models. The metastatic potential of NME2-depleted cells was remarkably diminished upon selective RNA-i-mediated silencing of vinculin. Together, we demonstrate that reduced NME2 levels lead to transcriptional de-repression of vinculin and regulate lung cancer metastasis. |*Gene Expression Regulation, Neoplastic [MESH] |*Genes, Tumor Suppressor [MESH] |Animals [MESH] |Cell Line, Tumor [MESH] |Disease Progression [MESH] |Focal Adhesions/genetics [MESH] |Humans [MESH] |Lung Neoplasms/*genetics/metabolism/mortality/*secondary [MESH] |Mice, Nude [MESH] |NM23 Nucleoside Diphosphate Kinases/*metabolism [MESH] |Promoter Regions, Genetic [MESH] |Transcription, Genetic [MESH] |Vinculin/biosynthesis/*genetics [MESH]Non-metastatic 2 (NME2)-mediated suppression of lung cancer metastasis(epmc).pdf DeepDyve Pubget Overpricing