Emerging role of N6-methyladenosine RNA methylation in lung diseases

肺癌 生物 疾病 基因沉默 生物信息学 癌症 癌症研究 哮喘 慢性阻塞性肺病 医学 免疫学 病理 内科学 基因 遗传学
作者
Limin Xu,Lingyan Zhou,Chenxin Yan,Liqin Li
出处
期刊:Experimental Biology and Medicine [SAGE]
卷期号:247 (20): 1862-1872 被引量:11
标识
DOI:10.1177/15353702221128564
摘要

In recent years, with the increase of air pollution, smoking, aging, and respiratory infection, the incidence rate and mortality of lung diseases are increasing annually, which has become a major hazard to human health. N6-methyladenosine (m6A) RNA methylation is the most abundant modifications in eukaryotes, and such modified RNA can be specifically recognized and combined by m6A recognition proteins and then mediate RNA splicing, maturation, enucleation, degradation, and translation. More and more studies have revealed that the m6A modification is involved in the pathogenesis and development of some diseases; however, the mechanisms of m6A in lung diseases are poorly understood. In this review, we summarize the latest progress in the biological function of m6A modifications in lung diseases and discuss the potential therapeutic and prognostic strategies. The dysregulation of global m6A levels and m6A regulators may affect the occurrence and development of asthma, chronic obstructive pulmonary disease, lung cancer, and other lung diseases through inflammation and immune function. In lung cancer, this modification has an important impact on malignant cell proliferation, migration, invasion, and drug resistance. In addition, abnormally changed m6A-modified proteins in lung cancer tissue samples and circulating tumor cells (CTCs) may be used as diagnostic and prognostic markers of lung cancer. Models composed of multiple m6A regulators can be used to evaluate the risk prediction or prognosis of asthma and pulmonary fibrosis. In general, the in-depth study of m6A modifications is a frontier direction in disease research. It provides novel insights for understanding of the molecular mechanisms underlying disease occurrence, development, and drug resistance, as well as for the development of effective novel therapeutics.

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
Linzi完成签到,获得积分10
1秒前
山山而川完成签到,获得积分10
1秒前
2秒前
chase完成签到,获得积分10
2秒前
阳光的香芦完成签到,获得积分20
2秒前
linlinyilulvdeng完成签到,获得积分10
2秒前
adai完成签到,获得积分10
2秒前
碧蓝天晴完成签到,获得积分10
2秒前
舒适的平蓝完成签到,获得积分10
3秒前
3秒前
哈哈完成签到,获得积分10
4秒前
晓彦发布了新的文献求助10
4秒前
沉默的婴完成签到 ,获得积分10
4秒前
量子星尘发布了新的文献求助10
5秒前
KingWong完成签到,获得积分10
5秒前
5秒前
6秒前
积极的怜南完成签到,获得积分10
6秒前
完美世界应助biiii采纳,获得10
6秒前
Feegood完成签到,获得积分10
6秒前
多宝完成签到,获得积分10
7秒前
zzz完成签到,获得积分10
8秒前
杰小瑞发布了新的文献求助10
8秒前
麦芽发布了新的文献求助10
8秒前
teborlee完成签到,获得积分10
9秒前
123完成签到,获得积分10
9秒前
Hello~完成签到,获得积分10
9秒前
FF完成签到 ,获得积分10
10秒前
10秒前
咖啡质感完成签到,获得积分10
10秒前
10秒前
西柚西柚完成签到 ,获得积分10
10秒前
11秒前
11秒前
CodeCraft应助Lanky采纳,获得30
11秒前
务实的河马完成签到,获得积分10
11秒前
wisher完成签到 ,获得积分10
12秒前
cdragon发布了新的文献求助10
12秒前
guanghan完成签到,获得积分10
12秒前
火星上宛秋完成签到 ,获得积分10
12秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Binary Alloy Phase Diagrams, 2nd Edition 8000
Building Quantum Computers 800
Translanguaging in Action in English-Medium Classrooms: A Resource Book for Teachers 700
Natural Product Extraction: Principles and Applications 500
Exosomes Pipeline Insight, 2025 500
Qualitative Data Analysis with NVivo By Jenine Beekhuyzen, Pat Bazeley · 2024 500
热门求助领域 (近24小时)
化学 材料科学 生物 医学 工程类 计算机科学 有机化学 物理 生物化学 纳米技术 复合材料 内科学 化学工程 人工智能 催化作用 遗传学 数学 基因 量子力学 物理化学
热门帖子
关注 科研通微信公众号,转发送积分 5664967
求助须知:如何正确求助?哪些是违规求助? 4873787
关于积分的说明 15110464
捐赠科研通 4824067
什么是DOI,文献DOI怎么找? 2582622
邀请新用户注册赠送积分活动 1536541
关于科研通互助平台的介绍 1495147