亲爱的研友该休息了!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,伴您度过漫漫科研夜!身体可是革命的本钱,早点休息,好梦!

A novel nanoplatform-based circCSNK1G3 affects CBX7 protein and promotes glioma cell growth

胶质瘤 化学 细胞生长 细胞生物学 计算生物学 癌症研究 生物物理学 纳米技术 生物 生物化学 材料科学
作者
Cheng-Jie Qiu,Liangyun Hu,Jin Yang,Jiaojiao Cao,Ben-Gen Pei,Ranran Dai,Si‐Jian Pan
出处
期刊:International Journal of Biological Macromolecules [Elsevier BV]
卷期号:: 134025-134025
标识
DOI:10.1016/j.ijbiomac.2024.134025
摘要

Bioenvironmental and biological factors have the potential to contribute to the development of glioma, a type of brain tumor. Recent studies have suggested that a unique circular RNA called circCSNK1G3 could play a role in promoting the growth of glioma cells. It does this by stabilizing a specific microRNA called miR-181 and reducing the expression of a tumor-suppressor gene known as chromobox protein homolog 7 (CBX7). To further investigate circCSNK1G3 and its effects on glioma, we utilized a nanoplatform called adeno-associated virus (AAV)-RNAi.To explore the functional implications of circCSNK1G3, we employed siRNA to silence its expression. Along with these effects, the silencing of circCSNK1G3 led to a depletion of miR-181d and an upregulation of CBX7. When we introduced miR-181d mimics, which artificially increase the levels of miR-181d, the anti-glioma cell activity induced by circCSNK1G3 siRNA was almost completely reversed. Conversely, inhibiting miR-181d mimicked the effects of circCSNK1G3 silencing. Moreover, when we overexpressed circCSNK1G3 in glioma cells, we observed an elevation of miR-181d and a depletion of CBX7. We found that the growth of A172 xenografts (tumors) carrying circCSNK1G3 shRNA was significantly inhibited. In these xenograft tissues, we detected a depletion of circCSNK1G3 and miR-181d, as well as an upregulation of CBX7.

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
在水一方应助aaaaa888888888采纳,获得10
4秒前
5秒前
念一发布了新的文献求助10
8秒前
中船科技发布了新的文献求助10
11秒前
20秒前
爆米花应助念一采纳,获得10
20秒前
eeevaxxx完成签到 ,获得积分10
25秒前
冷清之发布了新的文献求助10
25秒前
28秒前
31秒前
中船科技完成签到,获得积分20
32秒前
45秒前
冷清之完成签到 ,获得积分10
53秒前
1分钟前
1分钟前
兔子发布了新的文献求助10
1分钟前
1分钟前
1分钟前
1分钟前
在水一方应助jie采纳,获得10
1分钟前
zhang发布了新的文献求助10
1分钟前
1分钟前
2分钟前
2分钟前
燕燕发布了新的文献求助20
2分钟前
慕青应助aaaaa888888888采纳,获得10
2分钟前
2分钟前
小马甲应助兔子采纳,获得10
2分钟前
2分钟前
2分钟前
兔子完成签到,获得积分10
2分钟前
2分钟前
2分钟前
2分钟前
morethanlee发布了新的文献求助30
2分钟前
jie发布了新的文献求助10
2分钟前
白小超人完成签到 ,获得积分10
2分钟前
小蘑菇应助aaaaa888888888采纳,获得10
3分钟前
molihuakai应助jie采纳,获得10
3分钟前
3分钟前
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
The Cambridge History of China: Volume 4, Sui and T'ang China, 589–906 AD, Part Two 1500
Cowries - A Guide to the Gastropod Family Cypraeidae 1200
Quality by Design - An Indispensable Approach to Accelerate Biopharmaceutical Product Development 800
Pulse width control of a 3-phase inverter with non sinusoidal phase voltages 777
Signals, Systems, and Signal Processing 610
Research Methods for Applied Linguistics: A Practical Guide 600
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 物理 内科学 复合材料 催化作用 物理化学 光电子学 电极 细胞生物学 基因 无机化学
热门帖子
关注 科研通微信公众号,转发送积分 6399261
求助须知:如何正确求助?哪些是违规求助? 8215044
关于积分的说明 17407538
捐赠科研通 5452582
什么是DOI,文献DOI怎么找? 2881820
邀请新用户注册赠送积分活动 1858293
关于科研通互助平台的介绍 1700300