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10.18632/oncotarget.7224 http://scihub22266oqcxt.onion/10.18632/oncotarget.7224 C4891128!4891128 !26863455     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26863455 &cmd=llinks): Failed to open stream: HTTP request failed! 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OLA1 contributes to epithelial-mesenchymal transition in lung cancer by modulating the GSK3?/snail/E-cadherin signaling |pdf=|usr=}}{{26863455 }} gab.com Text OLA1 contributes to epithelial-mesenchymal transition in lung cancer by modulating the GSK3 /snail/E-cadherin signaling JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26863455 #FOAvip Obg-like ATPase 1 (OLA1) belongs to the Obg family of P-loop NTPases, and may serve as a "molecular switch" regulating multiple cellular processes. Aberrant expression of OLA1 has been observed in several human malignancies. However, the role of OLA1 in cancer progression remains poorly understood. In this study, we used the Kaplan-Meier plotter search tool to show that increased expression of OLA1 mRNA was significantly associated with shorter overall survival in lung cancer patients. By immunohistochemical analysis we discovered that levels of OLA1 protein in lung cancer tissues were positively correlated with TNM stage and lymph node metastasis, but negatively correlated with the epithelial-mesenchymal transition (EMT) marker E-cadherin. Knockdown of OLA1 in a lung adenocarcinoma cell line rendered the cells more resistant to TGF-?-induced EMT and the accompanied repression of E-cadherin. Furthermore, our results demonstrated that OLA1 is a GSK3?-interacting protein and inhibits GSK3? activity by mediating its Ser9 phosphorylation. During EMT, OLA1 plays an important role in suppressing the GSK3?-mediated degradation of Snail protein, which in turn promotes downregulation of E-cadherin. These data suggest that OLA1 contributes to EMT by modulating the GSK3?/Snail/E-cadherin signaling, and its overexpression is associated with clinical progression and poor survival in lung cancer patients. Twit Text FOAVip OLA1 contributes to epithelial-mesenchymal transition in lung cancer by modulating the GSK3 /snail/E-cadherin signaling ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26863455 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26863455 #FOAvip English Wikipedia <ref>{{Cite pmid|26863455 }}</ref> OLA1 contributes to epithelial-mesenchymal transition in lung cancer by modulating the GSK3?/snail/E-cadherin signaling #MMPMID26863455 Bai L ; Yu Z ; Zhang J ; Yuan S ; Liao C ; Jeyabal PV ; Rubio V ; Chen H ; Li Y ; Shi ZZ Oncotarget 2016[Mar]; 7 (9 ): 10402-13 PMID26863455 show ga Obg-like ATPase 1 (OLA1) belongs to the Obg family of P-loop NTPases, and may serve as a "molecular switch" regulating multiple cellular processes. Aberrant expression of OLA1 has been observed in several human malignancies. However, the role of OLA1 in cancer progression remains poorly understood. In this study, we used the Kaplan-Meier plotter search tool to show that increased expression of OLA1 mRNA was significantly associated with shorter overall survival in lung cancer patients. By immunohistochemical analysis we discovered that levels of OLA1 protein in lung cancer tissues were positively correlated with TNM stage and lymph node metastasis, but negatively correlated with the epithelial-mesenchymal transition (EMT) marker E-cadherin. Knockdown of OLA1 in a lung adenocarcinoma cell line rendered the cells more resistant to TGF-?-induced EMT and the accompanied repression of E-cadherin. Furthermore, our results demonstrated that OLA1 is a GSK3?-interacting protein and inhibits GSK3? activity by mediating its Ser9 phosphorylation. During EMT, OLA1 plays an important role in suppressing the GSK3?-mediated degradation of Snail protein, which in turn promotes downregulation of E-cadherin. These data suggest that OLA1 contributes to EMT by modulating the GSK3?/Snail/E-cadherin signaling, and its overexpression is associated with clinical progression and poor survival in lung cancer patients. |Adenocarcinoma of Lung [MESH] |Adenocarcinoma/genetics/mortality/*pathology [MESH] |Adenosine Triphosphatases/genetics/*metabolism [MESH] |Aged [MESH] |Cadherins/*metabolism [MESH] |Cell Line, Tumor [MESH] |Epithelial-Mesenchymal Transition/*genetics [MESH] |Female [MESH] |GTP-Binding Proteins/genetics/*metabolism [MESH] |Glycogen Synthase Kinase 3 beta/*metabolism [MESH] |Humans [MESH] |Lung Neoplasms/genetics/mortality/*pathology [MESH] |Lymphatic Metastasis [MESH] |Male [MESH] |Neoplasm Staging [MESH] |Phosphorylation [MESH] |RNA Interference [MESH] |RNA, Messenger/biosynthesis [MESH] |RNA, Small Interfering/genetics [MESH] |Snail Family Transcription Factors/*metabolism [MESH]OLA1 contributes to epithelial-mesenchymal transition in lung cancer b(epmc).pdf DeepDyve Pubget Overpricing