Please use this identifier to cite or link to this item: http://hdl.handle.net/123456789/5551
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dc.contributor.authorBie, Qingli-
dc.contributor.authorZhang, Bin-
dc.contributor.authorSun, Caixia-
dc.contributor.authorJi, Xiaoyun-
dc.contributor.authorBarnie, Prince Amoah-
dc.contributor.authorQi, Chen-
dc.contributor.authorPeng, Jingjing-
dc.contributor.authorZhang, Danyi-
dc.contributor.authorZheng, Dong-
dc.contributor.authorZheng, Dong-
dc.contributor.authorSu, Zhaoliang-
dc.contributor.authorWang, Shengjun-
dc.contributor.authorXu, Huaxi-
dc.date.accessioned2021-06-29T14:35:46Z-
dc.date.available2021-06-29T14:35:46Z-
dc.date.issued2017-01-27-
dc.identifier.issn23105496-
dc.identifier.urihttp://hdl.handle.net/123456789/5551-
dc.description10p:, ill.en_US
dc.description.abstractMesenchymal stem cells are important cells in tumor microenvironment. We have previously demonstrated that IL-17B/IL-17RB signal promoted progression of gastric cancer. In this study, we further explored the effect of IL-17B on mesenchymal stem cells in tumor microenvironment and its impact on the tumor progression. The results showed that IL-17B induced the expression of stemness-related genes Nanog, Sox2, and Oct4 in mesenchymal stem cells and enhanced its tumor-promoting effect. The supernatant from cultured mesenchymal stem cells after treating with exogenous rIL-17B promoted the proliferation and migration of MGC-803, therefor suggesting that rIL-17B might promote mesenchymal stem cells to produce soluble factors. In addition, rIL-17B also activated the NF-κΒ, STAT3, β-catenin pathway in mesenchymal stem cells. Our data revealed a new mechanism that IL-17B enhanced the progression of gastric cancer by activating mesenchymal stem cellsen_US
dc.language.isoenen_US
dc.publisherUniversity of Cape Coasten_US
dc.subjectGastric canceren_US
dc.subjectIL-17B, mesenchymal stem cells (MSCs)en_US
dc.subjectStemnessen_US
dc.titleIL-17B activated mesenchymal stem cells enhance proliferation and migration of gastric cancer cellsen_US
dc.typeArticleen_US
Appears in Collections:Department of Biomedical & Forensic Sciences

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