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10.18632/oncotarget.3416 http://scihub22266oqcxt.onion/10.18632/oncotarget.3416 C4484471!4484471 !25895023     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25895023 &cmd=llinks): Failed to open stream: HTTP request failed! 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Metastasis-associated in colon cancer-1 promotes vasculogenic mimicry in gastric cancer by upregulating TWIST1/2 |pdf=|usr=}}{{25895023 }} gab.com Text Metastasis-associated in colon cancer-1 promotes vasculogenic mimicry in gastric cancer by upregulating TWIST1/2 JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=25895023 #FOAvip Vasculogenic mimicry (VM) is a blood supply modality that is strongly associated with the epithelial-mesenchymal transition (EMT), TWIST1 activation and tumor progression. We previously reported that metastasis-associated in colon cancer-1 (MACC1) induced the EMT and was associated with a poor prognosis of patients with gastric cancer (GC), but it remains unknown whether MACC1 promotes VM and regulates the TWIST signaling pathway in GC. In this study, we investigated MACC1 expression and VM by immunohistochemistry in 88 patients with stage IV GC, and also investigated the role of TWIST1 and TWIST2 in MACC1-induced VM by using nude mice with GC xenografts and GC cell lines. We found that the VM density was significantly increased in the tumors of patients who died of GC and was positively correlated with MACC1 immunoreactivity (p < 0.05). The 3-year survival rate was only 8.6% in patients whose tumors showed double positive staining for MACC1 and VM, whereas it was 41.7% in patients whose tumors were negative for both MACC1 and VM. Moreover, nuclear expression of MACC1, TWIST1, and TWIST2 was upregulated in GC tissues compared with matched adjacent non-tumorous tissues (p < 0.05). Overexpression of MACC1 increased TWIST1/2 expression and induced typical VM in the GC xenografts of nude mice and in GC cell lines. MACC1 enhanced TWIST1/2 promoter activity and facilitated VM, while silencing of TWIST1 or TWIST2 inhibited VM. Hepatocyte growth factor (HGF) increased the nuclear translocation of MACC1, TWIST1, and TWIST2, while a c-Met inhibitor reduced these effects. These findings indicate that MACC1 promotes VM in GC by regulating the HGF/c-Met-TWIST1/2 signaling pathway, which means that MACC1 and this pathway are potential new therapeutic targets for GC. Twit Text FOAVip Metastasis-associated in colon cancer-1 promotes vasculogenic mimicry in gastric cancer by upregulating TWIST1/2 ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=25895023 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25895023 #FOAvip English Wikipedia <ref>{{Cite pmid|25895023 }}</ref> Metastasis-associated in colon cancer-1 promotes vasculogenic mimicry in gastric cancer by upregulating TWIST1/2 #MMPMID25895023 Wang L ; Lin L ; Chen X ; Sun L ; Liao Y ; Huang N ; Liao W Oncotarget 2015[May]; 6 (13 ): 11492-506 PMID25895023 show ga Vasculogenic mimicry (VM) is a blood supply modality that is strongly associated with the epithelial-mesenchymal transition (EMT), TWIST1 activation and tumor progression. We previously reported that metastasis-associated in colon cancer-1 (MACC1) induced the EMT and was associated with a poor prognosis of patients with gastric cancer (GC), but it remains unknown whether MACC1 promotes VM and regulates the TWIST signaling pathway in GC. In this study, we investigated MACC1 expression and VM by immunohistochemistry in 88 patients with stage IV GC, and also investigated the role of TWIST1 and TWIST2 in MACC1-induced VM by using nude mice with GC xenografts and GC cell lines. We found that the VM density was significantly increased in the tumors of patients who died of GC and was positively correlated with MACC1 immunoreactivity (p < 0.05). The 3-year survival rate was only 8.6% in patients whose tumors showed double positive staining for MACC1 and VM, whereas it was 41.7% in patients whose tumors were negative for both MACC1 and VM. Moreover, nuclear expression of MACC1, TWIST1, and TWIST2 was upregulated in GC tissues compared with matched adjacent non-tumorous tissues (p < 0.05). Overexpression of MACC1 increased TWIST1/2 expression and induced typical VM in the GC xenografts of nude mice and in GC cell lines. MACC1 enhanced TWIST1/2 promoter activity and facilitated VM, while silencing of TWIST1 or TWIST2 inhibited VM. Hepatocyte growth factor (HGF) increased the nuclear translocation of MACC1, TWIST1, and TWIST2, while a c-Met inhibitor reduced these effects. These findings indicate that MACC1 promotes VM in GC by regulating the HGF/c-Met-TWIST1/2 signaling pathway, which means that MACC1 and this pathway are potential new therapeutic targets for GC. |*Neovascularization, Pathologic [MESH] |Adenocarcinoma/blood supply/genetics/*metabolism/mortality/secondary [MESH] |Animals [MESH] |Cell Line, Tumor [MESH] |Epithelial-Mesenchymal Transition [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Hepatocyte Growth Factor/pharmacology [MESH] |Heterografts [MESH] |Kaplan-Meier Estimate [MESH] |Mice, Inbred NOD [MESH] |Mice, Nude [MESH] |Mice, SCID [MESH] |Neoplasm Staging [MESH] |Nuclear Proteins/genetics/*metabolism [MESH] |Promoter Regions, Genetic [MESH] |Protein Kinase Inhibitors/pharmacology [MESH] |Proto-Oncogene Proteins c-met/antagonists & inhibitors/metabolism [MESH] |RNA Interference [MESH] |Repressor Proteins/genetics/*metabolism [MESH] |Signal Transduction [MESH] |Stomach Neoplasms/blood supply/genetics/*metabolism/mortality/pathology [MESH] |Time Factors [MESH] |Trans-Activators [MESH] |Transcription Factors/genetics/*metabolism [MESH] |Transcription, Genetic [MESH] |Transfection [MESH] |Twist-Related Protein 1/genetics/*metabolism [MESH]Metastasis-associated in colon cancer-1 promotes vasculogenic mimicry (epmc).pdf DeepDyve Pubget Overpricing