B-Myb participated in ionizing radiation-induced apoptosis and cell cycle arrest in human glioma cells
B-Myb participated in ionizing radiation-induced apoptosis and cell cycle arrest in human glioma cells
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B-Myb 参与电离辐射诱导的人胶质瘤细胞凋亡和细胞周期停滞
DOI：
10.1016/j.bbrc.2021.08.014
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发表时间：
2021
影响因子：
3.1
通讯作者：
Zhongqin Liang
中科院分区：
文献类型：
--
作者：
Xiao Shen;Huimin Cao;Ying Zhu;Yifan Zhao;Yali liu;Wenqing Zuo;Fang Lin;Zhongqin Liang
作为对人神经胶质瘤的常见治疗，报道了电离辐射（IR）导致细胞周期。然而，IR诱导的异常细胞周期的基本机制在很大程度上尚不清楚。在这里。我们发现，IR引起了B-MYB和与细胞周期相关蛋白的表达升高，以及U251细胞而不是U87细胞中的G2/M.shase停滞。然而，通过小型干扰，B-MYB敲除RNA改善了由Ir.further分析引起的细胞周期相关蛋白的增加和G2/M期的停滞，表明B-MYB的降低增强了U251细胞对IR的敏感性对IR的敏感性。免疫沉淀（IP）和染色质免疫沉淀（CHIP）测定结果表明，突变体p53和SP1通过不同的机制调节B-MYB的表达。这项研究不仅阐明了B-Myb在IR诱导的细胞周期交替中的作用，但也提供了洞察力的洞察力。
As a common treatment of human glioma, ionizing radiation (IR) was reported to result in cell cycle.arrest. However, the mechanisms underlying IR-induced abnormal cell cycle remain largely unclear. Here.we found that IR caused an elevated expression of B-Myb and cell cycle-related proteins, as well as G2/M.phase arrest in U251 cells instead of U87 cells. However, the knockdown of B-Myb by small interfering.RNAs ameliorated the increasing of cell cycle-related proteins and G2/M phase arrest induced by IR..Further analysis demonstrated that decreased-B-Myb enhanced the sensitivity of U251 cells to IR..Moreover, the establishment of H1299 cell line proved that B-Myb expression was associated with the.status of p53. Immunoprecipitation (IP) and chromatin immunoprecipitation (CHIP) assay results indicated that mutant p53 and SP1 regulated the expression of B-Myb via different mechanisms. This study.not only elucidated the role of B-Myb in IR-induced cell cycle alternation, but also provided insight into.mechanism of B-Myb expression