Regulation of Gene Expression by N-methyladenosine in Cancer

N6-甲基腺苷 生物 甲基转移酶 RNA甲基化 基因表达 基因 甲基化 基因表达调控 调节器 癌症 计算生物学 功能(生物学) 核糖核酸 细胞生物学 遗传学 癌症研究
作者
Jun Liu,Bryan T. Harada,Chuan He
出处
期刊:Trends in Cell Biology [Elsevier BV]
卷期号:29 (6): 487-499 被引量:184
标识
DOI:10.1016/j.tcb.2019.02.008
摘要

m6A is the most abundant mRNA modification and it regulates many aspects of RNA metabolism, including RNA splicing, export, translation, and decay. Numerous recent studies indicate an important role for m6A in regulating gene expression in multiple physiologic processes, such as stress responses, stem cell differentiation, gametogenesis, and T cell homeostasis. Aberrant m6A mRNA methylation, through the altered expression of m6A writer, eraser, or reader proteins, has also been associated with several cancers. m6A has been reported to affect gene expression in cancer cells through many different pathways. In some studies, increased m6A methylation appears to contribute to cancer cell tumorigenicity by enhancing translation of oncogenes or degrading tumor suppressor genes. Other studies observe that m6A helps inhibit the expression of oncogenes, suggesting tumor suppressing roles for m6A methylation. As the most abundant mRNA modification in eukaryotic cells, N6-methyladenosine (m6A) has recently emerged as an important regulator of gene expression. m6A modification can be deposited by m6A methyltransferases, removed by m6A demethylases, and recognized by different reader proteins. Numerous lines of evidence have shown that m6A methylation plays critical roles regulating gene expression in development and disease. In this review, we summarize the molecular and cellular function of m6A and highlight some key results which demonstrate the role of m6A in various cancers. Finally, we discuss future directions for research into m6A and its effects in cancer and the potential for targeting RNA modification in cancer treatment. As the most abundant mRNA modification in eukaryotic cells, N6-methyladenosine (m6A) has recently emerged as an important regulator of gene expression. m6A modification can be deposited by m6A methyltransferases, removed by m6A demethylases, and recognized by different reader proteins. Numerous lines of evidence have shown that m6A methylation plays critical roles regulating gene expression in development and disease. In this review, we summarize the molecular and cellular function of m6A and highlight some key results which demonstrate the role of m6A in various cancers. Finally, we discuss future directions for research into m6A and its effects in cancer and the potential for targeting RNA modification in cancer treatment.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
why发布了新的文献求助10
刚刚
2秒前
智博36发布了新的文献求助10
3秒前
CodeCraft应助huimin采纳,获得10
3秒前
赫连涵柏完成签到,获得积分0
4秒前
6秒前
5cdc发布了新的文献求助10
6秒前
8秒前
waiting完成签到 ,获得积分10
10秒前
wyb发布了新的文献求助10
10秒前
丘比特应助智博36采纳,获得10
10秒前
10秒前
hzy完成签到,获得积分10
13秒前
矿泉水发布了新的文献求助10
13秒前
chever应助嘟嘟采纳,获得20
14秒前
英姑应助研新采纳,获得10
14秒前
深情安青应助maozhehai29999采纳,获得10
15秒前
思源应助struggling2026采纳,获得10
16秒前
田様应助Try采纳,获得10
16秒前
16秒前
annie完成签到,获得积分10
17秒前
领导范儿应助qazcy采纳,获得10
17秒前
18秒前
18秒前
顾矜应助fatcat采纳,获得30
19秒前
大个应助志豪采纳,获得10
20秒前
勤劳的涑完成签到,获得积分20
20秒前
挣扎的学渣完成签到,获得积分10
20秒前
王鑫发布了新的文献求助10
22秒前
江胜虎发布了新的文献求助10
22秒前
CodeCraft应助wyb采纳,获得10
22秒前
LXY发布了新的文献求助10
22秒前
23秒前
23秒前
hahu完成签到,获得积分10
23秒前
24秒前
25秒前
25秒前
lumen发布了新的文献求助10
25秒前
所所应助科研通管家采纳,获得10
25秒前
高分求助中
Разработка метода ускоренного контроля качества электрохромных устройств 500
Chinesen in Europa – Europäer in China: Journalisten, Spione, Studenten 500
Arthur Ewert: A Life for the Comintern 500
China's Relations With Japan 1945-83: The Role of Liao Chengzhi // Kurt Werner Radtke 500
Two Years in Peking 1965-1966: Book 1: Living and Teaching in Mao's China // Reginald Hunt 500
Epigenetic Drug Discovery 500
Politiek-Politioneele Overzichten van Nederlandsch-Indië. Bronnenpublicatie, Deel II 1929-1930 300
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 物理 生物化学 纳米技术 计算机科学 化学工程 内科学 复合材料 物理化学 电极 遗传学 量子力学 基因 冶金 催化作用
热门帖子
关注 科研通微信公众号,转发送积分 3819495
求助须知:如何正确求助?哪些是违规求助? 3362505
关于积分的说明 10417189
捐赠科研通 3080626
什么是DOI,文献DOI怎么找? 1694656
邀请新用户注册赠送积分活动 814719
科研通“疑难数据库(出版商)”最低求助积分说明 768403