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10.1186/s12943-017-0629-4 http://scihub22266oqcxt.onion/10.1186/s12943-017-0629-4 C5372323!5372323 !28356111     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28356111 &cmd=llinks): Failed to open stream: HTTP request failed! 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Tumor-derived CXCL5 promotes human colorectal cancer metastasis through activation of the ERK/Elk-1/Snail and AKT/GSK3?/?-catenin pathways |pdf=|usr=}}{{28356111 }} gab.com Text Tumor-derived CXCL5 promotes human colorectal cancer metastasis through activation of the ERK/Elk-1/Snail and AKT/GSK3 / -catenin pathways JO: Mol Cancer http://www.kidney.de/pget.php?&tw=1&pmid=28356111 #FOAvip BACKGROUND: Metastasis is a major cause of death in human colorectal cancer patients. However, the contribution of chemokines in the tumor microenvironment to tumor metastasis is not fully understood. METHODS: Herein, we examinined several chemokines in colorectal cancer patients using chemokine ELISA array. Immunohistochemistry was used to detect expression of CXCL5 in colorectal cancer patients tissues. Human HCT116 and SW480 cell lines stably transfected with CXCL5, shCXCL5 and shCXCR2 lentivirus plasmids were used in our in vitro study. Immunoblot, immunofluorescence and transwell assay were used to examine the molecular biology and morphological changes in these cells. In addition, we used nude mice to detect the influence of CXCL5 on tumor metastasis in vivo. RESULTS: We found that CXCL5 was overexpressed in tumor tissues and associated with advanced tumor stage as well as poor prognosis in colorectal cancer patients. We also demonstrated that CXCL5 was primarily expressed in the tumor cell cytoplasm and cell membranes, which may indicate that the CXCL5 was predominantly produced by cancer epithelial cells instead of fibroblasts in the tumor mesenchyme. Additionally, overexpression of CXCL5 enhanced the migration and invasion of colorectal cancer cells by inducing the epithelial-mesenchymal transition (EMT) through activation of the ERK/Elk-1/Snail pathway and the AKT/GSK3?/?-catenin pathway in a CXCR2-dependent manner. The silencing of Snail and ?-catenin attenuated CXCL5/CXCR2-enhanced cell migration and invasion in vitro. The elevated expression of CXCL5 can also potentiate the metastasis of colorectal cancer cells to the liver in vivo in nude mice intrasplenic injection model. CONCLUSION: In conclusion, our findings support CXCL5 as a promoter of colorectal cancer metastasis and a predictor of poor clinical outcomes in colorectal cancer patients. Twit Text FOAVip Tumor-derived CXCL5 promotes human colorectal cancer metastasis through activation of the ERK/Elk-1/Snail and AKT/GSK3 / -catenin pathways ????Mol Cancer http://www.kidney.de/pget.php?&tw=1&pmid=28356111 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28356111 #FOAvip English Wikipedia <ref>{{Cite pmid|28356111 }}</ref> Tumor-derived CXCL5 promotes human colorectal cancer metastasis through activation of the ERK/Elk-1/Snail and AKT/GSK3?/?-catenin pathways #MMPMID28356111 Zhao J ; Ou B ; Han D ; Wang P ; Zong Y ; Zhu C ; Liu D ; Zheng M ; Sun J ; Feng H ; Lu A Mol Cancer 2017[Mar]; 16 (1 ): 70 PMID28356111 show ga BACKGROUND: Metastasis is a major cause of death in human colorectal cancer patients. However, the contribution of chemokines in the tumor microenvironment to tumor metastasis is not fully understood. METHODS: Herein, we examinined several chemokines in colorectal cancer patients using chemokine ELISA array. Immunohistochemistry was used to detect expression of CXCL5 in colorectal cancer patients tissues. Human HCT116 and SW480 cell lines stably transfected with CXCL5, shCXCL5 and shCXCR2 lentivirus plasmids were used in our in vitro study. Immunoblot, immunofluorescence and transwell assay were used to examine the molecular biology and morphological changes in these cells. In addition, we used nude mice to detect the influence of CXCL5 on tumor metastasis in vivo. RESULTS: We found that CXCL5 was overexpressed in tumor tissues and associated with advanced tumor stage as well as poor prognosis in colorectal cancer patients. We also demonstrated that CXCL5 was primarily expressed in the tumor cell cytoplasm and cell membranes, which may indicate that the CXCL5 was predominantly produced by cancer epithelial cells instead of fibroblasts in the tumor mesenchyme. Additionally, overexpression of CXCL5 enhanced the migration and invasion of colorectal cancer cells by inducing the epithelial-mesenchymal transition (EMT) through activation of the ERK/Elk-1/Snail pathway and the AKT/GSK3?/?-catenin pathway in a CXCR2-dependent manner. The silencing of Snail and ?-catenin attenuated CXCL5/CXCR2-enhanced cell migration and invasion in vitro. The elevated expression of CXCL5 can also potentiate the metastasis of colorectal cancer cells to the liver in vivo in nude mice intrasplenic injection model. CONCLUSION: In conclusion, our findings support CXCL5 as a promoter of colorectal cancer metastasis and a predictor of poor clinical outcomes in colorectal cancer patients. |*Signal Transduction [MESH] |Animals [MESH] |Cell Line, Tumor [MESH] |Cell Movement [MESH] |Cell Proliferation [MESH] |Chemokine CXCL5/genetics/*metabolism [MESH] |Cluster Analysis [MESH] |Colorectal Neoplasms/genetics/*metabolism/*pathology [MESH] |Disease Models, Animal [MESH] |Epithelial-Mesenchymal Transition [MESH] |Extracellular Signal-Regulated MAP Kinases/metabolism [MESH] |Gene Expression Profiling [MESH] |Glycogen Synthase Kinase 3 beta/metabolism [MESH] |Heterografts [MESH] |Humans [MESH] |Liver Neoplasms/secondary [MESH] |Mice [MESH] |Models, Biological [MESH] |Prognosis [MESH] |Proto-Oncogene Proteins c-akt/metabolism [MESH] |Receptors, Interleukin-8B/metabolism [MESH] |Snail Family Transcription Factors/metabolism [MESH] |beta Catenin/metabolism [MESH]Tumor-derived CXCL5 promotes human colorectal cancer metastasis throug(epmc).pdf DeepDyve Pubget Overpricing