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K-RasG12V/T35S -ERK1/2 pathway regulates H2BS14ph through Mst1 to facilitate the advancement of breast cancer cells.
Biofactors ( IF 4.734 ) Pub Date : 2019-11-28 , DOI: 10.1002/biof.1589
Gang Bao,Wei Pan,Jianjun Huang,Tian Zhou

Breast cancer is a common cancer and becomes a severe healthy problem among females. Ras-ERK pathway and H2B phosphorylation at serine 14 (H2BS14ph) was involved in some cancers. Our research probed the feasible relationship between Ras-ERK1/2 and H2BS14ph in breast cancer cells and the underlying mechanism. MCF7 cells were transfected with RasG12V/T35S plasmid, and H2BS14ph, ERK1/2, Mst1, and MDM2 expression were evaluated through executing western blot. MTT, soft-agar colony formation, flow cytometry, and Transwell assays were applied for delving the functions of H2BS14 in MCF7 cells behavior. ERK1/2 pathway downstream factors and Mst1 expression was appraised via RT-PCR. The ChIP assay was utilized for detecting the relation between Ras and ERK1/2-downstream factors. We found that, RasG12V/T35S inhibited H2BS14ph expression while upregulated phospher-ERK1/2. In addition, RasG12V/T35S promoted MCF7 cell viability, colony numbers and migration, while H2BS14ph presented the opposite results. Transfection with RasG12V/T35S and cotransfection with RasG12V/T35S and H2BS14ph altered the expression of ERK1/2 downstream factors in an opposite direction. Additionally, RasG12V/T35S -ERK1/2 triggered H2BS14ph repression was concerned with MDM2-adjusted Mst1 degradation. Conclusions, RasG12V/T35S -ERK1/2 accelerated the development of breast cancer via mediating H2BS14ph by MDM2-modulated Mst1 degradation.
更新日期:2019-11-28

 

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