TRIM31 is upregulated in hepatocellular carcinoma and promotes disease progression by inducing ubiquitination of TSC1–TSC2 complex

生物 癌症研究 TSC2 mTORC1型 肝细胞癌 泛素 TSC1 肿瘤进展 肝癌 癌变 泛素连接酶 细胞生物学 PI3K/AKT/mTOR通路 下调和上调 癌症 信号转导 遗传学 基因
作者
Pengbo Guo,Xiaoxiao Ma,Wei Zhao,Wanwan Huai,Tianjiao Li,Yumin Qiu,Yahui Zhang,Lihui Han
出处
期刊:Oncogene [Springer Nature]
卷期号:37 (4): 478-488 被引量:108
标识
DOI:10.1038/onc.2017.349
摘要

Tripartite motif (TRIM) 31 is a member of the tripartite motif-containing protein family, and TRIM family proteins are involved in a broad range of biological and pathological processes. However, the role of TRIM31 in hepatocellular carcinoma (HCC) progression is not known. Here we demonstrated that TRIM31 expression was significantly upregulated in liver cancer tissues compared with paired distal non-cancerous liver tissues from HCC patients, and its overexpression was significantly correlated with advanced disease status. Both gain and loss of function assay verified that TRIM31 promoted the malignant behaviors of HCC cells through overactivation of mammalian target of rapamycin complex1 (mTORC1) pathway. We further demonstrated that TRIM31 exerted its oncogenic effect by directly interacting with the tuberous sclerosis complex (TSC) 1 and TSC2 complex, the upstream suppressor of mTORC1 pathway, and promoting the E3 ligase-mediated K48-linked ubiquitination and degradation of this complex. In conclusion, this study demonstrated TRIM31 could promote HCC progression by targeting TSC1-TSC2 complex for degradation and further overactivating mTORC1 pathway. Thus, it revealed a novel molecular mechanism of HCC progression and indicated a potential therapeutic strategy against HCC by targeting TRIM31.
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
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
CodeCraft的应助被李洁采纳,获得10
1秒前
科研通AI6.4的应助被www采纳,获得10
1秒前
2秒前
2秒前
2秒前
5EN完成签到,获得积分10
4秒前
xing_xing的应助被黄梓同采纳,获得20
5秒前
李y梅子完成签到 ,获得积分10
5秒前
东东完成签到,获得积分10
6秒前
fanfanqieqie发布了新的文献求助30
6秒前
alqb发布了新的文献求助80
6秒前
8秒前
SY发布了新的文献求助10
8秒前
9秒前
小鱼儿发布了新的文献求助10
9秒前
9秒前
东起欧发布了新的文献求助10
10秒前
11秒前
jyliu完成签到,获得积分10
11秒前
Dy发布了新的文献求助10
14秒前
14秒前
zimengzhu发布了新的文献求助10
14秒前
LZ发布了新的文献求助10
15秒前
柒柒完成签到 ,获得积分10
15秒前
16秒前
shi完成签到,获得积分10
16秒前
渡人舟的应助被low采纳,获得10
17秒前
Daleth完成签到,获得积分10
17秒前
英姑的应助被满天星采纳,获得10
18秒前
乐乐的应助被佘尉采纳,获得10
18秒前
19秒前
WHTTTTT发布了新的文献求助10
19秒前
直率的醉冬完成签到,获得积分10
21秒前
我能私信骂你吗的应助被YUNI采纳,获得10
22秒前
gougoudy完成签到,获得积分10
23秒前
junjiecheng1完成签到,获得积分10
23秒前
25秒前
26秒前
满天星完成签到,获得积分20
28秒前
29秒前
高分求助中
(应助此贴封号)通过应助OA文献获取积分 10000
Composite Materials Handbook Volume 1 - Revision H 1500
Rosenblum, Global Change Biology 800
Computational Chemical Reaction Engineering: Modeling, Simulation, and Design with MATLAB 600
Organizational Behavior 510
Management and the Arts 510
Decentring Leadership 400
热门求助领域 (近24小时)
化学 材料科学 医学 生物 计算机科学 工程类 纳米技术 内科学 物理 有机化学 化学工程 生物化学 复合材料 光电子学 细胞生物学 心理学 量子力学 催化作用 物理化学 电极
热门帖子
关注 科研通微信公众号,转发送积分 7807833
求助须知:如何正确求助?哪些是违规求助? 9340435
关于积分的说明 20501465
捐赠科研通 7400063
什么是DOI,文献DOI怎么找? 3328446
关于科研通互助平台的介绍 2475375
邀请新用户注册赠送积分活动 2346849