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!

MiR-654-3p targets SRC to suppress tumor growth in non-small cell lung cancer

肺癌 原癌基因酪氨酸蛋白激酶Src 癌症研究 生物 内科学 肿瘤科 癌症 医学 受体
作者
M. Pang,Yongjie Jiang,Yuyan Huang,Bi Ren,Liping He,Jiang Li
出处
期刊:Cellular and Molecular Biology [Cellular and Molecular Biology Association]
卷期号:69 (4): 157-163 被引量:2
标识
DOI:10.14715/cmb/2023.69.4.25
摘要

Around the world, cancer-related death is primarily caused by lung cancer all the time. MiR-654-3p plays an outstanding role in the development of cancer, but the mechanism of miR-654-3p in non-small cell lung cancer (NSCLC) is uncertain. For this purpose, a quantitative real-time polymerase chain reaction(qRT-PCR) was carried out to detect the expression of miR-654-3p and SRC mRNA. Western blot was used to estimate the level of SRC protein. The mimics enhanced miR-654-3p, while inhibitors knocked it down. Functional experiments were performed to evaluate the proliferation and migration capacities of cells. Flow cytometry assay was utilized to measure apoptosis rates and cell cycles of cells. TargetScan bioinformatics database was queried to identify the probable target gene for miR-654-3p. Dual-fluorescence assay was implemented to verify whether miR-654-3p targets SRC. Subcutaneous tumorigenesis was used to estimate the function of miR-654-3p in vivo. Results showed that low expression of miR-654-3p was found in NSCLC tissues and cells. Up-regulated miR-654-3p suppressed cell proliferation and migration, promoted apoptosis, and blocked cells in the G1 phase, while down-regulated miR-654-3p created the opposite results. Dual-fluorescence assay confirmed that miR-654-3p was directly bound to SRC. Compared with the control group, the effects of miR-654-3p were neutralized in the group, which was co-transfected with miR-654-3p mimics and SRC over-expression plasmids. In vivo, the tumor volume in the LV-miR-654-3p group was smaller than that in the control group. It was concluded that miR-654-3p acts in an anti-cancer role and suppresses tumor progression via regulating SRC, which lays a theoretical foundation for targeted therapy of NSCLC. MiR-654-3p is expected to be a new miRNA-based therapeutic target.
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
量子星尘发布了新的文献求助10
2秒前
4秒前
nanfang完成签到 ,获得积分10
13秒前
17秒前
18秒前
19秒前
19秒前
19秒前
共享精神应助ceeray23采纳,获得20
19秒前
Lendar完成签到 ,获得积分10
21秒前
24秒前
明亮猫咪发布了新的文献求助10
30秒前
炙热的夜雪完成签到 ,获得积分10
31秒前
Jasper应助hehehehe采纳,获得10
35秒前
Lucas应助完美的流沙采纳,获得10
35秒前
41秒前
小太阳完成签到,获得积分10
42秒前
46秒前
49秒前
草上飞完成签到 ,获得积分10
51秒前
hehehehe发布了新的文献求助10
54秒前
54秒前
hehehehe完成签到,获得积分10
1分钟前
ffff完成签到 ,获得积分10
1分钟前
yingying发布了新的文献求助10
1分钟前
量子星尘发布了新的文献求助10
1分钟前
canan发布了新的文献求助10
1分钟前
1分钟前
kajikaji完成签到,获得积分10
1分钟前
江姜酱先生完成签到,获得积分10
1分钟前
1分钟前
咕咕风发布了新的文献求助10
1分钟前
咕咕风完成签到,获得积分20
1分钟前
脑洞疼应助lf采纳,获得30
1分钟前
科研通AI5应助忧伤的风华采纳,获得10
1分钟前
flow完成签到,获得积分10
1分钟前
1分钟前
lf发布了新的文献求助30
2分钟前
苗条的小蜜蜂完成签到 ,获得积分10
2分钟前
orixero应助科研通管家采纳,获得30
2分钟前
高分求助中
A new approach to the extrapolation of accelerated life test data 1000
Picture Books with Same-sex Parented Families: Unintentional Censorship 700
ACSM’s Guidelines for Exercise Testing and Prescription, 12th edition 500
Nucleophilic substitution in azasydnone-modified dinitroanisoles 500
不知道标题是什么 500
Indomethacinのヒトにおける経皮吸収 400
Phylogenetic study of the order Polydesmida (Myriapoda: Diplopoda) 370
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 3976619
求助须知:如何正确求助?哪些是违规求助? 3520720
关于积分的说明 11204567
捐赠科研通 3257359
什么是DOI,文献DOI怎么找? 1798716
邀请新用户注册赠送积分活动 877897
科研通“疑难数据库(出版商)”最低求助积分说明 806613