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10.1038/onc.2015.365 http://scihub22266oqcxt.onion/10.1038/onc.2015.365 C4850112!4850112 !26434583     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26434583 &cmd=llinks): Failed to open stream: HTTP request failed! 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Atypical role of sprouty in colorectal cancer: sprouty repression inhibits epithelial-mesenchymal transition |pdf=|usr=}}{{26434583 }} gab.com Text Atypical role of sprouty in colorectal cancer: sprouty repression inhibits epithelial-mesenchymal transition JO: Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=26434583 #FOAvip Sprouty (SPRY) appears to act as a tumor suppressor in cancer, whereas we demonstrated that SPRY2 functions as a putative oncogene in colorectal cancer (CRC) (Oncogene, 2010, 29: 5241-5253). We investigated the mechanisms by which SPRY regulates epithelial-mesenchymal transition (EMT) in CRC. SPRY1 and SPRY2 mRNA transcripts were significantly upregulated in human CRC. Suppression of SPRY2 repressed AKT2 and EMT-inducing transcription factors and significantly increased E-cadherin expression. Concurrent downregulation of SPRY1 and SPRY2 also increased E-cadherin and suppressed mesenchymal markers in colon cancer cells. An inverse expression pattern between AKT2 and E-cadherin was established in a human CRC tissue microarray. SPRY2 negatively regulated miR-194-5p that interacts with AKT2 3' untranslated region. Mir-194 mimics increased E-cadherin expression and suppressed cancer cell migration and invasion. By confocal microscopy, we demonstrated redistribution of E-cadherin to plasma membrane in colon cancer cells transfected with miR-194. Spry1(-/-) and Spry2(-/-) double mutant mouse embryonic fibroblasts exhibited decreased cell migration while acquiring several epithelial markers. In CRC, SPRY drive EMT and may serve as a biomarker of poor prognosis. Twit Text FOAVip Atypical role of sprouty in colorectal cancer: sprouty repression inhibits epithelial-mesenchymal transition ????Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=26434583 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26434583 #FOAvip English Wikipedia <ref>{{Cite pmid|26434583 }}</ref> Atypical role of sprouty in colorectal cancer: sprouty repression inhibits epithelial-mesenchymal transition #MMPMID26434583 Zhang Q ; Wei T ; Shim K ; Wright K ; Xu K ; Palka-Hamblin HL ; Jurkevich A ; Khare S Oncogene 2016[Jun]; 35 (24 ): 3151-62 PMID26434583 show ga Sprouty (SPRY) appears to act as a tumor suppressor in cancer, whereas we demonstrated that SPRY2 functions as a putative oncogene in colorectal cancer (CRC) (Oncogene, 2010, 29: 5241-5253). We investigated the mechanisms by which SPRY regulates epithelial-mesenchymal transition (EMT) in CRC. SPRY1 and SPRY2 mRNA transcripts were significantly upregulated in human CRC. Suppression of SPRY2 repressed AKT2 and EMT-inducing transcription factors and significantly increased E-cadherin expression. Concurrent downregulation of SPRY1 and SPRY2 also increased E-cadherin and suppressed mesenchymal markers in colon cancer cells. An inverse expression pattern between AKT2 and E-cadherin was established in a human CRC tissue microarray. SPRY2 negatively regulated miR-194-5p that interacts with AKT2 3' untranslated region. Mir-194 mimics increased E-cadherin expression and suppressed cancer cell migration and invasion. By confocal microscopy, we demonstrated redistribution of E-cadherin to plasma membrane in colon cancer cells transfected with miR-194. Spry1(-/-) and Spry2(-/-) double mutant mouse embryonic fibroblasts exhibited decreased cell migration while acquiring several epithelial markers. In CRC, SPRY drive EMT and may serve as a biomarker of poor prognosis. |Adaptor Proteins, Signal Transducing/genetics/metabolism [MESH] |Animals [MESH] |Antigens, CD [MESH] |Cadherins/biosynthesis/metabolism [MESH] |Colorectal Neoplasms/genetics/*metabolism/*pathology [MESH] |Epithelial-Mesenchymal Transition [MESH] |Female [MESH] |Humans [MESH] |Intracellular Signaling Peptides and Proteins/genetics/*metabolism [MESH] |Membrane Proteins/genetics/*metabolism [MESH] |Mice [MESH] |Phosphoproteins/genetics/*metabolism [MESH] |Protein Serine-Threonine Kinases [MESH] |Proto-Oncogene Proteins c-akt/blood/metabolism [MESH] |Transfection [MESH]Atypical role of sprouty in colorectal cancer: sprouty repression inhi(epmc).pdf DeepDyve Pubget Overpricing