METTL13在肿瘤中的研究进展  

Progress of METTL13 Research in Tumors

作　　者：刘玉婵 杨勇莉[2] 李研 

机构地区：[1]青海大学研究生院,青海 西宁 [2]青海大学附属医院,青海 西宁

出　　处：《临床医学进展》2022年第5期4924-4928,共5页Advances in Clinical Medicine

摘　　要：蛋白质甲基转移酶样13 (METTL13)编码蛋白质Faint expression innormal tissues,aberrant over-expression in tumors (FEAT),位于染色体1q24.3,具有双甲基转移酶的特性。在大多数人类癌症中异常高表达,但在正常组织中弱表达。miR-16是FEAT的直接调节因子,miR-16直接识别并结合FEAT mRNA转录本的3’-UTR,从而抑制FEAT翻译。研究表明,FEAT在体内具有高度致癌作用。METTL13的异常调节与几种类型的癌症有关,但其确切机制尚不完全清楚。GEO图谱数据库中的全基因组连锁分析表明,人类METTL13基因的遗传变异与肿瘤恶性程度、肿瘤转移、癌症进展、化疗敏感性和微卫星不稳定性有关。本文系统回顾了与METTL13相关文献,就METTL13在肿瘤中的研究进展作一综述。The protein methyltransferase-like 13 (METTL13) encodes the protein Faint expression in normal tissues, aberrant overexpression in tumors (FEAT), located on chromosome 1q24.3, with dual me-thyltransferase properties. It is aberrantly highly expressed in most human cancers but weakly ex-pressed in normal tissues. miR-16 is a direct regulator of FEAT, and miR-16 directly recognizes and binds to the 3’-UTR of FEAT mRNA transcripts, thereby inhibiting FEAT translation. Studies have shown that FEAT is highly oncogenic in vivo. Aberrant regulation of METTL13 has been associated with several types of cancer, but the exact mechanism is not fully understood. Genome-wide linkage analysis in the GEO Atlas database suggests that genetic variation in the human METTL13 gene is associated with tumor malignancy, tumor metastasis, cancer progression, chemotherapy sensitivity, and microsatellite instability. In this paper, we systematically review the literature related to METTL13 and present a review on the progress of METTL13 research in tumors.

关 键 词：METTL13 FEAT蛋白 miR-16 肿瘤 

分 类 号：R730.2[医药卫生—肿瘤]