MUM1L1 as a Tumor Suppressor and Potential Biomarker in OvarianCancer: Evidence from Bioinformatics Analysis and Basic Experiments

卵巢癌 基因敲除 生物 生物标志物 生存分析 癌症研究 基因 抑制器 癌症 生物信息学 内科学 医学 遗传学
作者
Lu Zhang,Xue Wu,Xue Fan,Hao Ai
出处
期刊:Combinatorial Chemistry & High Throughput Screening [Bentham Science Publishers]
卷期号:26 (14): 2487-2501 被引量:7
标识
DOI:10.2174/1386207326666230301141912
摘要

Background: Ovarian cancer (OC) is the most prevalent gynecologic malignancy, with high mortality rates. However, its pathogenesis remains unclear. The current study aimed to explore potential biomarkers and suppressor genes for diagnosing and treating OC. Methods: Biochemical and bioinformatics approaches were used to detect differentially expressed genes (DEGs) in ovarian tissues via integration analysis. Kaplan-Meier plot analysis was performed to assess progression-free survival and overall survival according to DEGs. Then, we constructed a protein-protein interaction (PPI) network based on data from the STRING database to identify the related target genes of DEGs. Finally, DEGs regulating the proliferation, migration, and invasion of SKOV3 cell lines were validated via in vitro experiments. Results: Four DEGs (MUM1L1, KLHDC8A, CRYGD, and GREB1) with enriched expression in ovarian tissues were explicitly expressed in the ovary based on an analysis of all human proteins. MUM1L1 had high specificity, and its expression was higher in normal ovarian tissues than in OC tissues. Kaplan-Meier plot analysis showed that a high MUM1L1 expression was associated with longer progression-free survival and overall survival in OC. Based on the PPI analysis results, CBLN4, CBLN1, PTH2R, TMEM255B, and COL23A1 were associated with MUM1L1. In vitro studies revealed that MUM1L1 overexpression decreased the proliferation, migration, and invasion ability of SKOV3 cell lines. Meanwhile, MUM1L1 knockdown had contrasting results. Conclusion: MUM1L1 is a tumor suppressor gene and is a potential biomarker for diagnosing and treating OC.
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
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
彭于晏应助weiteng采纳,获得10
1秒前
Aesias完成签到,获得积分10
2秒前
2秒前
老李头发布了新的文献求助10
3秒前
000完成签到,获得积分10
3秒前
zyl发布了新的文献求助10
3秒前
3秒前
Chi应助海天使采纳,获得10
4秒前
小马甲应助小小牛马采纳,获得10
6秒前
6秒前
wwyyiiiiizz完成签到,获得积分20
7秒前
Sesenta1完成签到,获得积分10
8秒前
轻松白卉发布了新的文献求助10
8秒前
小蘑菇应助Leo采纳,获得10
8秒前
8秒前
脑洞疼应助佳佳采纳,获得10
10秒前
舍不得你发布了新的文献求助10
11秒前
11秒前
星辰大海应助梦wei采纳,获得10
13秒前
14秒前
天天快乐应助幸运鹅采纳,获得10
14秒前
肥猪完成签到 ,获得积分10
14秒前
weiteng发布了新的文献求助10
14秒前
15秒前
15秒前
CCC完成签到,获得积分10
16秒前
麦辣鸡翅完成签到,获得积分10
16秒前
笑点低的小懒虫完成签到,获得积分10
17秒前
18秒前
orixero应助大眼瞪小眼采纳,获得10
18秒前
小6s完成签到,获得积分10
19秒前
暖若安阳完成签到,获得积分10
19秒前
20秒前
LiuHX发布了新的文献求助10
20秒前
20秒前
kuikichu完成签到,获得积分10
20秒前
20秒前
memaclee完成签到,获得积分10
21秒前
是YN呀发布了新的文献求助10
22秒前
高分求助中
Principles of Economics, 11th Edition 10000
University Physics with Modern Physics, 16th edition 10000
(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
Arthritis and Related Conditions, An Issue of Orthopedic Clinics 1000
Development of a Bridge Weigh-In-Motion System: A technology to convert the bridge response to the passage of traffic into data on vehicle configurations, speeds, times of travel and weights 1000
ズームレンズの光学設計に関する研究 800
Fundamentals of Pharmaceutical and Biologics Regulations: A Global Perspective, Second Edition 700
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 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7292601
求助须知:如何正确求助?哪些是违规求助? 8911614
关于积分的说明 18865272
捐赠科研通 6959721
什么是DOI,文献DOI怎么找? 3209667
关于科研通互助平台的介绍 2379150
邀请新用户注册赠送积分活动 2185608