已入深夜,您辛苦了!由于当前在线用户较少,发布求助请尽量完整的填写文献信息,科研通机器人24小时在线,伴您度过漫漫科研夜!祝你早点完成任务,早点休息,好梦!

LncRNA OR3A4 participates in the angiogenesis of hepatocellular carcinoma through modulating AGGF1/akt/mTOR pathway

血管生成 癌症研究 PI3K/AKT/mTOR通路 蛋白激酶B 肿瘤进展 肝细胞癌 癌症 医学 生物 肿瘤科 内科学 信号转导 生物化学
作者
Wei Li,Qiang Fu,Wenling Man,Huanqing Guo,Po Song Yang
出处
期刊:European Journal of Pharmacology [Elsevier BV]
卷期号:849: 106-114 被引量:26
标识
DOI:10.1016/j.ejphar.2019.01.049
摘要

Hepatocellular carcinoma (HCC), as the commonest type in liver cancer, is in urgent need for better treatment target due to its high mortality and poor prognosis. The involvement of angiogenesis in HCC has been identified by multiple studies, but the underlying mechanism remains unclear. Long non-coding RNAs (LncRNAs) have been reported to regulate numerous cancers, including HCC. LncRNA-OR3A4 has been reported to exert oncogenic and angiogenetic functions in gastric cancer, but its role in HCC hasn’t been elucidated. Present study aimed to uncover the biological role of OR3A4 in tumor progression and angiogenesis in HCC. The upregulation of OR3A4 in HCC tissues and cell lines and its prognostic significance were first identified. Loss-of-function assays, including CCK-8, transwell and tube formation assay, validated OR3A4 as a promoter for HCC progression and angiogenesis. The association of OR3A4 and AGGF1 with HCC and poor prognosis was identified by qRT-PCR and Kaplan-Meier analysis. Western blotting and spearman's correlation curve verified the effect of OR3A4 on AGGF1 level and their positive association. Rescue assays revealed that OR3A4 promoted cancer progression and angiogenesis in HCC via AGGF1/akt/mTOR. Together, present study revealed OR3A4 as a novel prognostic target for HCC, which regulated tumor progression and angiogenesis through AGGF1/akt/mTOR pathway.
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
6秒前
kangwer完成签到,获得积分10
6秒前
科研通AI5应助lull采纳,获得10
9秒前
13秒前
葶ting完成签到 ,获得积分10
13秒前
14秒前
丘比特应助落小兜采纳,获得10
14秒前
19秒前
粒子耶发布了新的文献求助10
21秒前
lulu完成签到,获得积分10
22秒前
23秒前
24秒前
wangxin发布了新的文献求助10
25秒前
26秒前
动漫大师发布了新的文献求助30
27秒前
28秒前
28秒前
传统的故事关注了科研通微信公众号
29秒前
暖暖完成签到,获得积分10
29秒前
31秒前
TaoJ发布了新的文献求助10
32秒前
32秒前
32秒前
小二郎应助悠嘻嘻采纳,获得10
33秒前
科研小农民应助一堃采纳,获得10
34秒前
258完成签到,获得积分10
36秒前
落小兜完成签到,获得积分20
36秒前
37秒前
深情安青应助Hh采纳,获得10
39秒前
SiRui_Wang关注了科研通微信公众号
40秒前
42秒前
乐观的莆发布了新的文献求助10
42秒前
美丽的又菡完成签到,获得积分10
44秒前
45秒前
45秒前
45秒前
47秒前
一堃完成签到,获得积分10
47秒前
勤劳糜发布了新的文献求助10
50秒前
jasmine发布了新的文献求助10
50秒前
高分求助中
Les Mantodea de Guyane Insecta, Polyneoptera 2500
Technologies supporting mass customization of apparel: A pilot project 450
A Field Guide to the Amphibians and Reptiles of Madagascar - Frank Glaw and Miguel Vences - 3rd Edition 400
A China diary: Peking 400
Brain and Heart The Triumphs and Struggles of a Pediatric Neurosurgeon 400
Cybersecurity Blueprint – Transitioning to Tech 400
Mixing the elements of mass customisation 400
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 物理 生物化学 纳米技术 计算机科学 化学工程 内科学 复合材料 物理化学 电极 遗传学 量子力学 基因 冶金 催化作用
热门帖子
关注 科研通微信公众号,转发送积分 3784705
求助须知:如何正确求助?哪些是违规求助? 3329891
关于积分的说明 10243654
捐赠科研通 3045221
什么是DOI,文献DOI怎么找? 1671596
邀请新用户注册赠送积分活动 800484
科研通“疑难数据库(出版商)”最低求助积分说明 759416