miR-93-5p suppresses cellular senescence by directly targeting Bcl-w and p21.

作者: Jae Yeon Choi , Hyun Jin Shin , In Hwa Bae

DOI: 10.1016/J.BBRC.2018.10.010

关键词: OncogeneHistone H3Cancer cellmicroRNACell growthCancer researchBiologySenescenceContext (language use)Angiogenesis

摘要: Cellular senescence, a distinctive type of irreversible growth arrest, develops in response to various stimuli. Bcl-w, an oncogene and member the Bcl-2 family, has been reported promote tumorigenicity cancer cells. Here, we sought explore potential role Bcl-w premature which received relatively little research attention. Our findings demonstrate that enhances activity senescence-associated β-galactosidase (SA-β-gal) promotes histone H3 tri-methylation at lysine 9 (H3K9me3) expressions p53, Notch2, p21, p16-hallmarks senescent phenotype-in human U251 glioblastoma H460 lung carcinoma It is also known microRNAs (miRNAs) regulate processes related tumor development, such as cell proliferation, differentiation, survival, metabolism, inflammation, invasion, angiogenesis, senescence. In this context, found miR-93-5p inhibited cellular senescence by directly suppressing p21 expressions. Collectively, these suggest targeting miR-93-5p-regulated may be useful strategy for preventing

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