Protein Arginine Methyltransferases (PRMTs): Orchestrators of Cancer Pathogenesis, Immunotherapy Dynamics, and Drug Resistance

甲基转移酶 发病机制 免疫疗法 精氨酸 癌症 抗药性 免疫系统 蛋白质精氨酸甲基转移酶5 药品 生物 医学 癌症研究 甲基化 免疫学 药理学 遗传学 氨基酸 基因
作者
Yihang Gao,Chuanqi Feng,Jinjin Ma,Yan Qiao
出处
期刊:Biochemical Pharmacology [Elsevier]
卷期号:: 116048-116048
标识
DOI:10.1016/j.bcp.2024.116048
摘要

Protein Arginine Methyltransferases (PRMTs) are a family of enzymes regulating protein arginine methylation, which is a post-translational modification crucial for various cellular processes. Recent studies have highlighted the mechanistic role of PRMTs in cancer pathogenesis, immunotherapy, and drug resistance. PRMTs are involved in diverse oncogenic processes, including cell proliferation, apoptosis, and metastasis. They exert their effects by methylation of histones, transcription factors, and other regulatory proteins, resulting in altered gene expression patterns. PRMT-mediated histone methylation can lead to aberrant chromatin remodeling and epigenetic changes that drive oncogenesis. Additionally, PRMTs can directly interact with key signaling pathways involved in cancer progression, such as the PI3K/Akt and MAPK pathways, thereby modulating cell survival and proliferation. In the context of cancer immunotherapy, PRMTs have emerged as critical regulators of immune responses. They modulate immune checkpoint molecules, including programmed cell death protein 1 (PD-1), through arginine methylation. Drug resistance is a significant challenge in cancer treatment, and PRMTs have been implicated in this phenomenon. PRMTs can contribute to drug resistance through multiple mechanisms, including the epigenetic regulation of drug efflux pumps, altered DNA damage repair, and modulation of cell survival pathways. In conclusion, PRMTs play critical roles in cancer pathogenesis, immunotherapy, and drug resistance. In this overview, we have endeavored to illuminate the mechanistic intricacies of PRMT-mediated processes. Shedding light on these aspects will offer valuable insights into the fundamental biology of cancer and establish PRMTs as promising therapeutic targets.
最长约 10秒,即可获得该文献文件

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
wanci应助赫鲁晓夫采纳,获得10
刚刚
2秒前
Mike001发布了新的文献求助10
2秒前
Lucas应助LjDwm9采纳,获得10
3秒前
4秒前
Mike001发布了新的文献求助50
4秒前
7秒前
乐乐应助xlb采纳,获得10
9秒前
9秒前
周同学发布了新的文献求助10
10秒前
彩色甜瓜发布了新的文献求助10
11秒前
honey完成签到,获得积分10
12秒前
13秒前
张店烹鱼宴完成签到,获得积分10
13秒前
14秒前
Lws发布了新的文献求助10
14秒前
从容芮应助科研通管家采纳,获得50
14秒前
SciGPT应助科研通管家采纳,获得10
14秒前
14秒前
周同学完成签到,获得积分10
15秒前
16秒前
糖醋里脊加醋完成签到,获得积分10
16秒前
洋洋发布了新的文献求助10
16秒前
LjDwm9发布了新的文献求助10
17秒前
yahonyoyoyo发布了新的文献求助10
20秒前
20秒前
不倦应助taipingyang采纳,获得10
20秒前
jxp完成签到,获得积分10
22秒前
慕青应助yahonyoyoyo采纳,获得10
24秒前
科目三应助清脆珍采纳,获得10
24秒前
LjDwm9完成签到,获得积分10
26秒前
胖胖橘发布了新的文献求助10
32秒前
大力的草莓完成签到,获得积分10
33秒前
34秒前
36秒前
大意的饼干完成签到 ,获得积分10
36秒前
streamerz完成签到,获得积分10
37秒前
38秒前
39秒前
40秒前
高分求助中
Manual of Clinical Microbiology, 4 Volume Set (ASM Books) 13th Edition 1000
Teaching Social and Emotional Learning in Physical Education 900
The three stars each : the Astrolabes and related texts 550
Boris Pesce - Gli impiegati della Fiat dal 1955 al 1999 un percorso nella memoria 500
Chinese-English Translation Lexicon Version 3.0 500
Recherches Ethnographiques sue les Yao dans la Chine du Sud 500
[Lambert-Eaton syndrome without calcium channel autoantibodies] 460
热门求助领域 (近24小时)
化学 材料科学 医学 生物 有机化学 工程类 生物化学 纳米技术 物理 内科学 计算机科学 化学工程 复合材料 遗传学 基因 物理化学 催化作用 电极 光电子学 量子力学
热门帖子
关注 科研通微信公众号,转发送积分 2399563
求助须知:如何正确求助?哪些是违规求助? 2100285
关于积分的说明 5295060
捐赠科研通 1828107
什么是DOI,文献DOI怎么找? 911224
版权声明 560133
科研通“疑难数据库(出版商)”最低求助积分说明 487058