N6-methyladenosine-dependent signalling in cancer progression and insights into cancer therapies

被引:0
作者
Fenghua Tan
Mengyao Zhao
Fang Xiong
Yumin Wang
Shanshan Zhang
Zhaojian Gong
Xiayu Li
Yi He
Lei Shi
Fuyan Wang
Bo Xiang
Ming Zhou
Xiaoling Li
Yong Li
Guiyuan Li
Zhaoyang Zeng
Wei Xiong
Can Guo
机构
[1] Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine,NHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism
[2] Central South University,Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education
[3] Cancer Research Institute,Department of Stomatology
[4] Central South University,Department of Oral and Maxillofacial Surgery
[5] Xiangya Hospital,Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Disease Genome Research Center
[6] Central South University,undefined
[7] the Second Xiangya Hospital,undefined
[8] Central South University,undefined
[9] The Third Xiangya Hospital,undefined
[10] Central South University,undefined
[11] Department of Medicine,undefined
[12] Dan L Duncan Comprehensive Cancer Center,undefined
[13] Baylor College of Medicine,undefined
来源
Journal of Experimental & Clinical Cancer Research | / 40卷
关键词
N6-methyladenosine; Signal transduction pathway; Cancer progression; Therapy; RNA fate;
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摘要
The N6-methyladenosine (m6A) modification is a dynamic and reversible epigenetic modification, which is co-transcriptionally deposited by a methyltransferase complex, removed by a demethylase, and recognized by reader proteins. Mechanistically, m6A modification regulates the expression levels of mRNA and nocoding RNA by modulating the fate of modified RNA molecules, such as RNA splicing, nuclear transport, translation, and stability. Several studies have shown that m6A modification is dysregulated in the progression of multiple diseases, especially human tumors. We emphasized that the dysregulation of m6A modification affects different signal transduction pathways and involves in the biological processes underlying tumor cell proliferation, apoptosis, invasion and migration, and metabolic reprogramming, and discuss the effects on different cancer treatment.
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