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机构地区:[1]苏州大学医学部放射医学与防护学院,苏州215123
出 处:《辐射研究与辐射工艺学报》2013年第1期1-5,共5页Journal of Radiation Research and Radiation Processing
基 金:国家自然科学基金(81172706);江苏高校优势学科建设工程资助项目(PAPD)资助
摘 要:miR-34a位于染色体1p36.23区,作用于多种靶基因。miR-34a的异常表达可诱发细胞凋亡、周期阻滞和细胞分化,也可降低肿瘤细胞的转移,被认为是一种肿瘤抑制因子。抑癌基因p53可以激活miR-34a,miR-34a也可反馈调节p53表达。电离辐射诱导的miR-34a异常表达在DNA损伤修复、细胞凋亡、细胞周期调节和细胞辐射敏感性中发挥重要作用。本文综述电离辐射诱导miR-34a的产生及其参与的生物学反应和调控机制。miR-34a resides in the region of chromosome lp36.23, which regulate a plethora of target genes. Ectopic miR-34a expression can induce apoptosis, cell cycle arrest and differentiation, meanwhile reduce migration of tumour cell which known as tumour inhibiting factor, p53 was shown a capability of activating miR-34a expression and miR-34a was also shown a feedback regulation to p53 gene in reverse. Ectopic expression of miR-34a induced by ionizing radiation plays an important role in DNA damage repair, apoptosis, cell cycle and cellular radiation sensitivity. This article reviews the progress in produce of miR-34a during ionizing radiation and its participation in biological response and relative mechanism in control.
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