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eIF3b和METTL3通过m 6A介导促进宫颈癌进展的作用机制及研究进展

Mechanism and research progress of eIF3b and METTL3 in promoting the progression of cervical cancer via the mediation of m 6A
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摘要 真核翻译起始因子3(eIF3)是由13个亚基组成的复合物,是目前已发现的eIFs中最大的真核翻译起始因子。eIF3b作为其关键亚基,在翻译起始的调控中具有举足轻重的作用。甲基转移酶样3(METTL3)是一种已知的具有催化活性的甲基转移酶,是甲基转移酶复合体的关键成分,其负责对N6-甲基腺苷(m^(6)A)进行甲基化修饰。近年来越来越多的研究表明,eIF3b、METTL3在多种人类恶性肿瘤中高表达,可通过m^(6)A介导产生联系。且研究发现eIF3b、METTL3均在宫颈癌中高表达,可促进宫颈癌细胞的增殖、侵袭、迁移,抑制细胞凋亡。文章主要就eIF3b、METTL3通过m^(6)A介导在宫颈癌发展中的具体作用机制以及研究进展进行综述。 Eukaryotic translation initiation factor 3(eIF3)is a complex composed of 13 subunits,and is the largest eukaryotic translation initiation factor discovered so far.As a key subunit,eIF3b plays a pivotal role in the regulation of translation initiation.Methyltransferase-like 3(METTL3)is a known methyltransferase with catalytic activity.It is a key component of the methyltransferase complex which is responsible for the methylation modification of N6-methyladenosine(m^(6)A).In recent years,more and more studies have shown that eIF3b and METTL3 are highly expressed in a variety of human malignant tumors,and can be mediated by m^(6)A.Studies have also found that eIF3b and METTL3 are highly expressed in cervical cancer,which can promote the proliferation,invasion and migration of cervical cancer cells and inhibit cell apoptosis.This article mainly reviews the specific mechanisms and research progress of eIF3b and METTL3 in the development of cervical cancer via the mediation of m^(6)A.
作者 范香 王逸斐 杨霓(综述) 朱鹏峰(审校) FAN Xiang;WANG Yifei;YANG Ni;ZHU Pengfeng(Department of Gynecology and Tumors,Changzhou Maternal and Child Health Care Hospital,Changzhou Medical Center,Nanjing Medical University,Changzhou 213000,Jiangsu,China)
出处 《医学研究与战创伤救治》 北大核心 2023年第9期1000-1004,共5页 Journal of Medical Research & Combat Trauma Care
基金 常州市卫生健康委员会重大课题项目(ZD202121) 常州市科技局应用基础研究计划项目(CJ20220251) 常州市“十四五”卫生健康高层次人才培养工程——拔尖人才(2022CZBJ085)。
关键词 真核翻译起始因子3b 甲基转移酶样3 N6-甲基腺苷 宫颈癌 eukaryotic translation initiation factor 3b methyltransferase-like 3 N6-methyladenosine cervical cancer
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