清晨好,您是今天最早来到科研通的研友!由于当前在线用户较少,发布求助请尽量完整地填写文献信息,科研通机器人24小时在线,伴您科研之路漫漫前行!

CtBP2 interacts with ZBTB18 to promote malignancy of glioblastoma

小发夹RNA 污渍 转染 分子生物学 邻近连接试验 基因敲除 癌症研究 细胞凋亡 细胞生长 生物 细胞生物学 化学
作者
Liang Chen,Lu Wang,Jun Qin,De-Sheng Wei
出处
期刊:Life Sciences [Elsevier BV]
卷期号:262: 118477-118477 被引量:3
标识
DOI:10.1016/j.lfs.2020.118477
摘要

To investigate how the interaction of CtBP2 with ZBTB18 affect glioblastoma (GBM). Western blotting was performed to detect CtBP2 and ZBTB18 expression in GBM and normal brain tissues (NBT). U-87 MG cells were transfected with ZBTB18 CRISPR activation plasmid, CtBP2 shRNA with/without ZBTB18 shRNA. The biological characteristics were detected by EdU assay, MTT, Wound-healing, Transwell, TUNEL staining, and Flow cytometry. Furthermore, U-87 MG cells transfected with CtBP2 shRNA and/or ZBTB18 shRNA were injected into the flank region of mice and the tumor volume was measured. The mRNA and protein expression was quantified by qRT-PCR or Western blotting. GBM tissues exhibited increased CtBP2 expression and decreased ZBTB18 expression, which demonstrated a negative correlation in GBM tissues and showed the combined effect on prognosis. Based on immunoprecipitation and immunofluorescence, there was an interaction between CtBP2 and ZBTB18 in U-87 MG cells. CtBP2 shRNA counteracted the effect of ZBTB18 shRNA on inhibiting U-87 MG cell apoptosis, as well as promoting cell proliferation and viability with increased EMT, invasion and migration. Meanwhile, CtBP2 shRNA interact with ZBTB18 to block cells at phase G0/G1 and suppress SHH-GLI1 pathway. CtBP2 shRNA decreased tumor volume, increase ZBTB18 expression in tumor tissues, and inhibit SHH-GLI1 pathway in mice, which could be reversed by ZBTB18 shRNA. CtBP2 elevation and ZBTB18 down-regulation were found in GBM, both of which were associated with prognosis of GBM patients. CtBP2 interacted with ZBTB18 to affect biological characteristics of GBM cells, and the tumor growth, which may be related to the SHH-GLI1 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
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

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
26秒前
不秃燃的小老弟完成签到 ,获得积分10
33秒前
科研通AI5应助科研通管家采纳,获得10
49秒前
1分钟前
桥西小河完成签到 ,获得积分10
1分钟前
生物材料完成签到,获得积分10
1分钟前
研友_8Yo3dn完成签到,获得积分10
1分钟前
糟糕的翅膀完成签到,获得积分10
1分钟前
青出于蓝蔡完成签到,获得积分10
1分钟前
追风发布了新的文献求助10
2分钟前
yshj完成签到 ,获得积分10
2分钟前
赘婿应助每㐬山风采纳,获得10
2分钟前
cy0824完成签到 ,获得积分10
3分钟前
负责以山完成签到 ,获得积分10
3分钟前
3分钟前
每㐬山风发布了新的文献求助10
3分钟前
烨枫晨曦完成签到,获得积分10
4分钟前
田様应助婼汐采纳,获得30
4分钟前
每㐬山风完成签到,获得积分20
4分钟前
4分钟前
4分钟前
荣安安发布了新的文献求助10
4分钟前
大个应助顺心的皓轩采纳,获得10
5分钟前
5分钟前
5分钟前
Arbor发布了新的文献求助10
5分钟前
5分钟前
顺心的皓轩完成签到,获得积分10
5分钟前
5分钟前
Arbor完成签到,获得积分10
6分钟前
6分钟前
Arbor发布了新的文献求助10
7分钟前
老石完成签到 ,获得积分10
7分钟前
末末完成签到 ,获得积分10
8分钟前
奶油布丁完成签到 ,获得积分10
8分钟前
科研通AI2S应助科研通管家采纳,获得10
8分钟前
9分钟前
婼汐发布了新的文献求助30
9分钟前
荣誉完成签到,获得积分0
9分钟前
CipherSage应助xakars采纳,获得10
10分钟前
高分求助中
The Mother of All Tableaux: Order, Equivalence, and Geometry in the Large-scale Structure of Optimality Theory 3000
Social Research Methods (4th Edition) by Maggie Walter (2019) 2390
A new approach to the extrapolation of accelerated life test data 1000
Problems of point-blast theory 400
北师大毕业论文 基于可调谐半导体激光吸收光谱技术泄漏气体检测系统的研究 390
Phylogenetic study of the order Polydesmida (Myriapoda: Diplopoda) 370
Robot-supported joining of reinforcement textiles with one-sided sewing heads 320
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 生物化学 物理 内科学 纳米技术 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 冶金 细胞生物学 免疫学
热门帖子
关注 科研通微信公众号,转发送积分 4001172
求助须知:如何正确求助?哪些是违规求助? 3540525
关于积分的说明 11278570
捐赠科研通 3278590
什么是DOI,文献DOI怎么找? 1808139
邀请新用户注册赠送积分活动 884356
科研通“疑难数据库(出版商)”最低求助积分说明 810260