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BAG2 Promotes Proliferation and Metastasis of Gastric Cancer via ERK1/2 Signaling and Partially Regulated by miR186

Bcl2-associated athanogene (BAG)2 as a co-chaperone has been demonstrated to be involved in tumor growth and metastasis, but its biological function in gastric cancer remains unknown. Here, we reported that BAG2 was highly expressed in gastric cancer cell lines and tissues, indicating poor prognosis...

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Detalles Bibliográficos
Autores principales: Sun, Lisha, Chen, Guanglei, Sun, Anqi, Wang, Zheng, Huang, Haibo, Gao, Ziming, Liang, Weitian, Liu, Caigang, Li, Kai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7005010/
https://www.ncbi.nlm.nih.gov/pubmed/32082999
http://dx.doi.org/10.3389/fonc.2020.00031
Descripción
Sumario:Bcl2-associated athanogene (BAG)2 as a co-chaperone has been demonstrated to be involved in tumor growth and metastasis, but its biological function in gastric cancer remains unknown. Here, we reported that BAG2 was highly expressed in gastric cancer cell lines and tissues, indicating poor prognosis. High expression of BAG2 was significantly associated with T stage and differentiation level of gastric cancer (P < 0.001). Functional experiments revealed that BAG2 knockdown in gastric cancer cells inhibited the proliferation, invasion and migration of cells through AKT/mTOR and extracellular regulated kinase (ERK) pathways. Proteomic analysis identified that BAG2 may be involved in the regulation of mitogen-activated protein kinase (MAPK) pathway. In addition, immunoprecipitation showed that BAG2 could bind to ERK1/2. Luciferase reporter assay and Western blot verified that BAG2 was down-regulated by miR186. Taken together, our findings may reveal the basic function of BAG2 and uncover a potential therapeutic target for gastric cancer.