Clinical significance of the ubiquitin ligase UBE3C in hepatocellular carcinoma revealed by exome sequencing

泛素连接酶 肝细胞癌 外显子组测序 外显子组 泛素 生物 DNA连接酶 遗传学 计算生物学 突变 基因
作者
Jia-Hao Jiang,Yanfeng Liu,Ai‐Wu Ke,Fangming Gu,Yu Yao,Zhi Dai,Qiang Gao,Guo‐Ming Shi,Boyi Liao,Youhua Xie,Jia Fan,Xiaowu Huang,Jian Zhou
出处
期刊:Hepatology [Lippincott Williams & Wilkins]
卷期号:59 (6): 2216-2227 被引量:58
标识
DOI:10.1002/hep.27012
摘要

UNLABELLED: Virus-induced hepatocarcinogenesis involves a series of histological developmental processes with the stepwise acquisition of several genetic changes that are necessary for the malignant transformation of hepatocytes. Although genetic alterations are known to be involved in the pathogenesis of hepatocellular carcinoma (HCC), little is known about the contributions of specific genes to this process. To gain insight into the genetic alterations involved in the neoplastic evolution from chronic hepatitis B virus infection to dysplastic nodules (DN) to HCC, we captured and sequenced the exomes of four DNA samples: one DN sample, two HCC samples, and one control peripheral blood sample from a single HCC patient. Mutations in the UBE3C gene (encoding ubiquitin ligase E3C) were observed in both tumor tissues. Then we resequenced the UBE3C gene in a cohort of 105 HCC patients and identified mutations in 17 out of a total of 106 (16.0%) HCC patients. The subsequent experiments showed that UBE3C promoted HCC progression by regulating HCC cells epithelial-mesenchymal transition. Clinically, a tissue microarray study of a cohort containing 323 HCC patients revealed that the overexpression of UBE3C in primary HCC tissues correlated with decreased survival (hazard ratio [HR] =1.657, 95% confidence interval [CI] =1.220-2.251, P=0.001) and early tumor recurrence (HR=1.653, 95% CI=1.227-2.228, P=0.001) in postoperative HCC patients. CONCLUSION: Our findings indicate that UBE3C is a candidate oncogene involved in tumor development and progression and therefore a potential therapeutic target in applicable HCC patients.

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
6666应助科研界年兽采纳,获得10
刚刚
CC发布了新的文献求助10
2秒前
皮皮完成签到,获得积分10
3秒前
小虫子完成签到,获得积分10
3秒前
3秒前
dulcetlemon完成签到,获得积分10
7秒前
安纳给tsunami的求助进行了留言
8秒前
Autaro完成签到,获得积分10
8秒前
azuretimm完成签到,获得积分10
10秒前
azuretimmq完成签到,获得积分10
10秒前
桃酥完成签到 ,获得积分10
10秒前
感性的苑博完成签到 ,获得积分10
10秒前
11秒前
Mississippiecho完成签到,获得积分10
11秒前
小宋完成签到,获得积分10
11秒前
科研通AI6.4应助一一采纳,获得10
13秒前
lipeng完成签到,获得积分10
14秒前
maowei完成签到,获得积分10
14秒前
MODRIC完成签到 ,获得积分10
14秒前
ww完成签到,获得积分10
15秒前
孟德尔吃豌豆完成签到,获得积分10
15秒前
11111111111111完成签到,获得积分10
16秒前
shiyi发布了新的文献求助10
16秒前
听风完成签到,获得积分10
17秒前
小八统治世界完成签到,获得积分10
17秒前
稳重的奇迹完成签到,获得积分10
18秒前
DayLight完成签到,获得积分10
20秒前
20秒前
幽默的煎饼完成签到,获得积分10
20秒前
bingbing完成签到,获得积分10
21秒前
机智的灵萱完成签到,获得积分10
21秒前
Y橙子完成签到,获得积分10
21秒前
小崔发布了新的文献求助10
21秒前
小黄小黄辉煌完成签到,获得积分10
22秒前
ZCX完成签到 ,获得积分10
23秒前
十六月夜完成签到,获得积分0
23秒前
杨超越完成签到,获得积分10
24秒前
w1完成签到,获得积分10
24秒前
cxjie320完成签到,获得积分0
24秒前
永不言弃完成签到 ,获得积分10
24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
Effects of Two Weeks of Red Light Therapy on Choroidal Thickness and Axial Length in Young Adults 700
Management and the Arts 510
Matrix Methods in Data Mining and Pattern Recognition Second Edition 510
The Neuroscience of Language 400
Common Foundations of American and East Asian Modernisation: From Alexander Hamilton to Junichero Koizumi 400
Too Much of Two Good Things: Investment Protection and Environmental Protection in International Law 260
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7673554
求助须知:如何正确求助?哪些是违规求助? 9240083
关于积分的说明 19903913
捐赠科研通 7243233
什么是DOI,文献DOI怎么找? 3285600
关于科研通互助平台的介绍 2443724
邀请新用户注册赠送积分活动 2287868