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
刚刚
1秒前
Yuki发布了新的文献求助10
1秒前
王哇噻完成签到 ,获得积分10
1秒前
Lee发布了新的文献求助10
1秒前
dajing发布了新的文献求助10
1秒前
2秒前
潇湘夜雨完成签到,获得积分10
2秒前
2秒前
2秒前
3秒前
kai发布了新的文献求助10
4秒前
4秒前
yue发布了新的文献求助30
4秒前
qing晴发布了新的文献求助10
4秒前
4秒前
5秒前
无限的南霜完成签到,获得积分10
5秒前
5秒前
6秒前
我是老大应助123qwe采纳,获得10
6秒前
6秒前
帅帅厅发布了新的文献求助10
6秒前
WNL发布了新的文献求助10
7秒前
shangshang发布了新的文献求助30
7秒前
8秒前
斯文智宸发布了新的文献求助10
8秒前
脑洞疼应助JLY采纳,获得10
8秒前
8秒前
橙色小瓶子完成签到,获得积分10
8秒前
直率海亦完成签到,获得积分10
8秒前
星辰大海应助科研通管家采纳,获得10
9秒前
9秒前
浮游应助科研通管家采纳,获得10
9秒前
李健应助科研通管家采纳,获得10
9秒前
薄雪草完成签到,获得积分10
9秒前
大个应助科研通管家采纳,获得10
9秒前
Orange应助郭小胖14采纳,获得10
9秒前
浮游应助科研通管家采纳,获得10
9秒前
一二应助科研通管家采纳,获得10
9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
Einführung in die Rechtsphilosophie und Rechtstheorie der Gegenwart 1500
NMR in Plants and Soils: New Developments in Time-domain NMR and Imaging 600
Electrochemistry: Volume 17 600
La cage des méridiens. La littérature et l’art contemporain face à la globalisation 577
Practical Invisalign Mechanics: Crowding 500
Practical Invisalign Mechanics: Deep Bite and Class II Correction 500
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 内科学 生物化学 物理 计算机科学 纳米技术 遗传学 基因 复合材料 化学工程 物理化学 病理 催化作用 免疫学 量子力学
热门帖子
关注 科研通微信公众号,转发送积分 4954553
求助须知:如何正确求助?哪些是违规求助? 4216890
关于积分的说明 13121171
捐赠科研通 3999023
什么是DOI,文献DOI怎么找? 2188625
邀请新用户注册赠送积分活动 1203758
关于科研通互助平台的介绍 1116092