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10.12659/msm.906945 http://scihub22266oqcxt.onion/10.12659/msm.906945 C5907830!5907830 !29628496     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29628496 &cmd=llinks): Failed to open stream: HTTP request failed! 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Ezrin/NF-?B Pathway Regulates EGF-induced Epithelial-Mesenchymal Transition (EMT), Metastasis, and Progression of Osteosarcoma |pdf=|usr=}}{{29628496 }} gab.com Text Ezrin/NF- B Pathway Regulates EGF-induced Epithelial-Mesenchymal Transition (EMT), Metastasis, and Progression of Osteosarcoma JO: Med Sci Monit http://www.kidney.de/pget.php?&tw=1&pmid=29628496 #FOAvip BACKGROUND Epithelial-mesenchymal transition (EMT) is responsible for metastasis of cancers, and NF-?B can promote tumor progression. Ezrin is an important molecule participating in EMT. However, whether Ezrin mediates NF-?B in EGF-induced osteosarcoma is unknown. MATERIAL AND METHODS Ezrin phosphorylation, NF-?B activation, and EGF-induced EMT were studied in MG63 and U20S cells with NF-?B inhibition, silencing, or over-expressing Ezrin. Cell morphology, proliferation, migration, and motility were analyzed. An osteosarcoma model was established in mice by injecting MG63 and U20S and reducing Ezrin. RESULTS With EGF induction in vitro, Ezrin Tyr353 and Thr567 were phosphorylated, and EMT, proliferation, migration, and motility of osteosarcoma cells were promoted. Silencing Ezrin suppressed and over-expressing Ezrin promoted the nuclear translocation of p65 and phosphorylated I?B? (p-I?B?) in EGF-induced osteosarcoma cells. NF-?B inhibitor blocked EGF-induced EMT in both cell types, as well as reserving cell morphology and suppressing proliferation, migration, and motility. In vivo, reducing Ezrin significantly suppressed metastasis of osteosarcoma xenografts, increased liver and lung weights, and activated NF-?B, which were both induced by EGF. CONCLUSIONS Ezrin/NF-?B regulated EGF-induced EMT, as well as progression and metastasis of osteosarcoma in vivo and in vitro. Ezrin/NF-?B may be a new therapeutic target to prevent osteosarcoma from deterioration. Twit Text FOAVip Ezrin/NF- B Pathway Regulates EGF-induced Epithelial-Mesenchymal Transition (EMT), Metastasis, and Progression of Osteosarcoma ????Med Sci Monit http://www.kidney.de/pget.php?&tw=1&pmid=29628496 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29628496 #FOAvip English Wikipedia <ref>{{Cite pmid|29628496 }}</ref> Ezrin/NF-?B Pathway Regulates EGF-induced Epithelial-Mesenchymal Transition (EMT), Metastasis, and Progression of Osteosarcoma #MMPMID29628496 Liu P ; Yang P ; Zhang Z ; Liu M ; Hu S Med Sci Monit 2018[Apr]; 24 (ä): 2098-2108 PMID29628496 show ga BACKGROUND Epithelial-mesenchymal transition (EMT) is responsible for metastasis of cancers, and NF-?B can promote tumor progression. Ezrin is an important molecule participating in EMT. However, whether Ezrin mediates NF-?B in EGF-induced osteosarcoma is unknown. MATERIAL AND METHODS Ezrin phosphorylation, NF-?B activation, and EGF-induced EMT were studied in MG63 and U20S cells with NF-?B inhibition, silencing, or over-expressing Ezrin. Cell morphology, proliferation, migration, and motility were analyzed. An osteosarcoma model was established in mice by injecting MG63 and U20S and reducing Ezrin. RESULTS With EGF induction in vitro, Ezrin Tyr353 and Thr567 were phosphorylated, and EMT, proliferation, migration, and motility of osteosarcoma cells were promoted. Silencing Ezrin suppressed and over-expressing Ezrin promoted the nuclear translocation of p65 and phosphorylated I?B? (p-I?B?) in EGF-induced osteosarcoma cells. NF-?B inhibitor blocked EGF-induced EMT in both cell types, as well as reserving cell morphology and suppressing proliferation, migration, and motility. In vivo, reducing Ezrin significantly suppressed metastasis of osteosarcoma xenografts, increased liver and lung weights, and activated NF-?B, which were both induced by EGF. CONCLUSIONS Ezrin/NF-?B regulated EGF-induced EMT, as well as progression and metastasis of osteosarcoma in vivo and in vitro. Ezrin/NF-?B may be a new therapeutic target to prevent osteosarcoma from deterioration. |Animals [MESH] |Bone Neoplasms/chemically induced/*metabolism/pathology [MESH] |Cell Line, Tumor [MESH] |Cell Movement/drug effects [MESH] |Cell Proliferation/drug effects [MESH] |Cytoskeletal Proteins/*metabolism [MESH] |Disease Models, Animal [MESH] |Disease Progression [MESH] |Epidermal Growth Factor/*pharmacology [MESH] |Epithelial-Mesenchymal Transition/drug effects [MESH] |Heterografts [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |NF-KappaB Inhibitor alpha/metabolism [MESH] |NF-kappa B/*metabolism [MESH] |Neoplasm Metastasis [MESH] |Osteosarcoma/chemically induced/*metabolism/pathology [MESH] |Phosphorylation [MESH]Ezrin/NF-?B Pathway Regulates EGF-induced Epithelial-Mesenchymal Trans(epmc).pdf DeepDyve Pubget Overpricing