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!祝你早点完成任务,早点休息,好梦!

LINC01133 regulates MARCKS expression via sponging miR-30d-5p to promote the development of lung squamous cell carcinoma

细胞凋亡 细胞生长 马尔克斯 下调和上调 流式细胞术 癌症研究 细胞 细胞生物学 荧光素酶 细胞迁移 生物 分子生物学 细胞培养 转染 信号转导 基因 蛋白激酶C 生物化学 遗传学
作者
Yajun Zhang,Woda Shi,Rongjin Chen,Yan Gu,Mengjie Zhao,Jianxiang Song,Zhan Shi,Jixiang Wu,Hui‐Wen Chang,Ming Liu
出处
期刊:Translational Oncology [Elsevier]
卷期号:44: 101931-101931
标识
DOI:10.1016/j.tranon.2024.101931
摘要

LncRNAs are vital regulators for lung squamous cell carcinoma (LUSC). However, the detailed role that LINC01133 plays in LUSC is unclear. This work sought to explore the potential function of LINC01133.Levels of LINC01133, miR-30d-5p, and MARCKS were separately tested in both tissues and cells using qRT-PCR. Proliferation was assessed through MTT experiment and apoptosis was detected upon flow cytometry. Transwell experiments were implemented to evaluate migratory and invasive abilities. The interaction between two genes was affirmed through luciferase reporter assay and RNA pull-down experiment. Western blotting measured the protein level of MARCKS. Animal models were established and tissues were taken for IHC analysis of MARCKS and Ki67.LINC01133 was elevated in LUSC and its downregulation could suppress proliferation, migration and invasion but induced apoptosis. LINC01133 interacted with and regulated the binding of miR-30d-5p to MARCKS. LINC01133/miR-30d-5p axis mediated proliferation, apoptosis, migration and invasion in LUSC cells, as well as modulated tumor growth in animal models. LINC01133 interacted with miR-30d-5p to modulate MARCKS expression, contributes to promoted cell proliferation, migration, invasion, and inhibited cell apoptosis in vitro, and promoted tumor growth in vivo. These findings could provide possible therapeutic targets in view of LUSC treatment in the future.

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
1秒前
1秒前
米米发布了新的文献求助10
1秒前
1秒前
2秒前
3秒前
yy发布了新的文献求助10
4秒前
4秒前
默默访冬发布了新的文献求助10
4秒前
传奇3应助YANGHAN采纳,获得10
5秒前
6秒前
6秒前
7秒前
蟹老板发布了新的文献求助20
7秒前
7秒前
小吕小吕发布了新的文献求助10
7秒前
8秒前
我666完成签到,获得积分10
8秒前
ruhemann发布了新的文献求助10
8秒前
8秒前
8秒前
Mountain完成签到 ,获得积分10
9秒前
ZZ发布了新的文献求助10
11秒前
11秒前
11秒前
12秒前
12秒前
wbYuan完成签到,获得积分10
13秒前
贪玩梦山完成签到,获得积分20
13秒前
yundong完成签到,获得积分10
13秒前
小二郎应助ruhemann采纳,获得10
14秒前
15秒前
15秒前
wwwww完成签到 ,获得积分10
15秒前
15秒前
小蘑菇应助科研通管家采纳,获得10
15秒前
cs发布了新的文献求助10
15秒前
共享精神应助科研通管家采纳,获得30
16秒前
16秒前
斯文败类应助科研通管家采纳,获得50
16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
Kinesiophobia : a new view of chronic pain behavior 3000
Les Mantodea de guyane 2500
Molecular Biology of Cancer: Mechanisms, Targets, and Therapeutics 2000
Standard: In-Space Storable Fluid Transfer for Prepared Spacecraft (AIAA S-157-2024) 1000
Signals, Systems, and Signal Processing 510
Discrete-Time Signals and Systems 510
热门求助领域 (近24小时)
化学 材料科学 生物 医学 工程类 计算机科学 有机化学 物理 生物化学 纳米技术 复合材料 内科学 化学工程 人工智能 催化作用 遗传学 数学 基因 量子力学 物理化学
热门帖子
关注 科研通微信公众号,转发送积分 5949372
求助须知:如何正确求助?哪些是违规求助? 7122874
关于积分的说明 15915784
捐赠科研通 5082594
什么是DOI,文献DOI怎么找? 2732556
邀请新用户注册赠送积分活动 1693166
关于科研通互助平台的介绍 1615632