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The endonuclease APE1 processes miR-92b formation, thereby regulating expression of the tumor suppressor LDLR in cervical cancer cells
Therapeutic Advances in Medical Oncology ( IF 4.3 ) Pub Date : 2019-07-10 , DOI: 10.1177/1758835919855859
Yi Sun 1 , Yun Feng 2 , Guiqian Zhang 3 , Ya Xu 3
Affiliation  

RNA damage induced by missing bases [e.g. by generation of apurinic/apyrimidinic (AP) sites], or by modification of bases (e.g. by oxidative damage), can alter RNA function and is increasingly found to participate in carcinogenesis.1 For instance, mRNA damaged by oxidation or AP-site formation can interfere with translational accuracy.1 In the case of microRNAs (miRNAs), oxidation can alter their regulatory activity, thus modifying expression of target genes.2 Consequently, degradation of damaged miRNAs in genotoxic environments can have significant repercussions in oncogenesis and for the development of chemoresistance in existing tumors.

中文翻译:

核酸内切酶 APE1 处理 miR-92b 的形成,从而调节肿瘤抑制因子 LDLR 在宫颈癌细胞中的表达

由缺失碱基引起的 RNA 损伤[例如通过产生无嘌呤/无嘧啶 (AP) 位点],或通过碱基修饰(例如通过氧化损伤)可以改变 RNA 功能,并且越来越多地被发现参与致癌作用。1例如,因氧化或 AP 位点形成而受损的 mRNA 会干扰翻译准确性。1对于 microRNA (miRNA),氧化可以改变它们的调节活性,从而改变靶基因的表达。2因此,基因毒性环境中受损 miRNA 的降解可能对肿瘤发生和现有肿瘤中化学抗性的发展产生重大影响。
更新日期:2019-07-10
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