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10.3892/mmr.2018.8976 http://scihub22266oqcxt.onion/10.3892/mmr.2018.8976 C6059661!6059661!29749455     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29749455&cmd=llinks): Failed to open stream: HTTP request failed! 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Anti-metastatic effects of Aidi on human esophageal squamous cell carcinoma by inhibiting epithelial-mesenchymal transition and angiogenesis |pdf=|usr=}}{{29749455}} gab.com Text Anti-metastatic effects of Aidi on human esophageal squamous cell carcinoma by inhibiting epithelial-mesenchymal transition and angiogenesis JO: Mol Med Rep http://www.kidney.de/pget.php?&tw=1&pmid=29749455 #FOAvip Aidi injection, a proprietary Chinese medicine, has been widely used for the treatment of cancer. However, its effects and potential mechanism in esophageal squamous cell carcinoma (ESCC) have not yet been characterized. The aim of the present study was to identify the mechanism underlying the anti-metastatic effects of treatment with Aidi. To test the effects and mechanism, EC9706 and KYSE70 cells were selected for in vitro experiments. In vivo, the anti-metastatic effects of Aidi injection on a nude mouse peritoneal metastasis model were examined, and the mechanisms were assessed with immunohistochemical staining. A cell proliferation assay demonstrated that treatment with more than 3 mg/ml Aidi for 24 or 48 h significantly inhibited the proliferation of EC9706 (P<0.01) and KYSE70 cells (P<0.05, P<0.01). Subsequent experiments assessed cell migration, invasion and vasculogenic mimicry (VM) formation, with 5-fluorouracil serving as a positive control. It was observed that treatment with Aidi inhibited cell migration, invasion and VM formation. Furthermore, it was identified that treatment with Aidi inhibited epithelial-mesenchymal transition (EMT) signaling and the expression of vascular endothelial growth factor A (VEGF-A) in EC9706 and KYSE70 cells, using western blotting. In the in vivo experiments, Aidi injection effectively suppressed tumor metastasis in the mouse tumor model. Additionally, the expression of vimentin and vascular endothelial growth factor was decreased, and the expression of cadherin-1 was increased in the tumor tissue. The present results suggested that treatment with Aidi may inhibit tumor metastasis in ESCC through the inhibition of EMT signaling and angiogenesis. Twit Text FOAVip Anti-metastatic effects of Aidi on human esophageal squamous cell carcinoma by inhibiting epithelial-mesenchymal transition and angiogenesis ????Mol Med Rep http://www.kidney.de/pget.php?&tw=1&pmid=29749455 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29749455 #FOAvip English Wikipedia <ref>{{Cite pmid|29749455}}</ref> Anti-metastatic effects of Aidi on human esophageal squamous cell carcinoma by inhibiting epithelial-mesenchymal transition and angiogenesis #MMPMID29749455 Shi Q; Diao Y; Jin F; Ding Z Mol Med Rep 2018[Jul]; 18 (1): 131-8 PMID29749455show ga Aidi injection, a proprietary Chinese medicine, has been widely used for the treatment of cancer. However, its effects and potential mechanism in esophageal squamous cell carcinoma (ESCC) have not yet been characterized. The aim of the present study was to identify the mechanism underlying the anti-metastatic effects of treatment with Aidi. To test the effects and mechanism, EC9706 and KYSE70 cells were selected for in vitro experiments. In vivo, the anti-metastatic effects of Aidi injection on a nude mouse peritoneal metastasis model were examined, and the mechanisms were assessed with immunohistochemical staining. A cell proliferation assay demonstrated that treatment with more than 3 mg/ml Aidi for 24 or 48 h significantly inhibited the proliferation of EC9706 (P<0.01) and KYSE70 cells (P<0.05, P<0.01). Subsequent experiments assessed cell migration, invasion and vasculogenic mimicry (VM) formation, with 5-fluorouracil serving as a positive control. It was observed that treatment with Aidi inhibited cell migration, invasion and VM formation. Furthermore, it was identified that treatment with Aidi inhibited epithelial-mesenchymal transition (EMT) signaling and the expression of vascular endothelial growth factor A (VEGF-A) in EC9706 and KYSE70 cells, using western blotting. In the in vivo experiments, Aidi injection effectively suppressed tumor metastasis in the mouse tumor model. Additionally, the expression of vimentin and vascular endothelial growth factor was decreased, and the expression of cadherin-1 was increased in the tumor tissue. The present results suggested that treatment with Aidi may inhibit tumor metastasis in ESCC through the inhibition of EMT signaling and angiogenesis. äAnti-metastatic effects of Aidi on human esophageal squamous cell carc(epmc).pdf DeepDyve Pubget Overpricing