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]
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
更新
大幅提高文件上传限制,最高150M (2024-4-1)

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
拼搏妙竹完成签到,获得积分10
刚刚
shi发布了新的文献求助10
刚刚
1秒前
春夏秋冬发布了新的文献求助10
3秒前
3秒前
haipronl发布了新的文献求助10
4秒前
Lucky完成签到,获得积分10
4秒前
4秒前
受伤的妙之应助发财小手采纳,获得10
4秒前
旺仔完成签到,获得积分10
5秒前
科研通AI2S应助Cc采纳,获得10
7秒前
就这样完成签到 ,获得积分10
7秒前
7秒前
c程序语言发布了新的文献求助30
7秒前
彭于晏完成签到,获得积分10
7秒前
加油呀完成签到,获得积分10
8秒前
小布丁完成签到,获得积分10
8秒前
8秒前
9秒前
田様应助神勇初瑶采纳,获得20
9秒前
10秒前
10秒前
11秒前
zxzx完成签到,获得积分10
11秒前
李小鑫吖发布了新的文献求助10
12秒前
seacnli完成签到,获得积分10
12秒前
12秒前
希望天下0贩的0应助LIUYI采纳,获得10
13秒前
小仙鱼发布了新的文献求助10
13秒前
末岛完成签到,获得积分10
13秒前
CipherSage应助我是砖家采纳,获得10
13秒前
13秒前
彳亍发布了新的文献求助10
13秒前
14秒前
lancerimpp完成签到,获得积分10
14秒前
15秒前
赵文伟发布了新的文献求助30
15秒前
科研通AI2S应助朴素幻柏采纳,获得10
16秒前
16秒前
16秒前
高分求助中
Evolution 10000
ISSN 2159-8274 EISSN 2159-8290 1000
Becoming: An Introduction to Jung's Concept of Individuation 600
Ore genesis in the Zambian Copperbelt with particular reference to the northern sector of the Chambishi basin 500
A new species of Coccus (Homoptera: Coccoidea) from Malawi 500
A new species of Velataspis (Hemiptera Coccoidea Diaspididae) from tea in Assam 500
PraxisRatgeber: Mantiden: Faszinierende Lauerjäger 500
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3160487
求助须知:如何正确求助?哪些是违规求助? 2811659
关于积分的说明 7892950
捐赠科研通 2470589
什么是DOI,文献DOI怎么找? 1315639
科研通“疑难数据库(出版商)”最低求助积分说明 630910
版权声明 602042