Validation of ESM1 Related to Ovarian Cancer and the Biological Function and Prognostic Significance

医学 血管生成 生物标志物 内科学 转移 肿瘤科 癌症 癌症研究 生物 遗传学
作者
Yukun Li,Tian Zeng,Guan Yang,Jue Liu,Nianchun Liao,Mengjie Wang,Ke-xin Chen,Xianyu Luo,Chang-ye Chen,Feifei Quan,Juan Wang,Qun-feng Zhang,Juan Zou
出处
期刊:International Journal of Biological Sciences [Ivyspring International Publisher]
卷期号:19 (1): 258-280 被引量:46
标识
DOI:10.7150/ijbs.66839
摘要

Background: Ovarian cancer (OC), a serious gynecological malignant disease, remains an enormous challenge in early diagnosis and medical treatment. Based on the GEO and TCGA databases in R language, endothelial cell-specific molecule 1 (ESM1) was confirmed separately with the bioinformatic analysis tool. ESM1 has been demonstrated to be upregulated in multiple cancer types, but the oncogenic mechanism by which ESM1 promotes OC is still largely unknown. Methods: In this study, we used WGCNA and random survival forest variable screening to filter out ESM1 in OC differentially expressed genes (DEGs). Next, we confirmed the mRNA and protein levels of ESM1 in OC samples via PCR and IHC. The correlation between the ESM1 level and clinical data of OC patients was further confirmed, including FIGO stage, lymph node metastasis, and recurrence. The role of ESM1 in OC development was explored by several functional experiments in vivo and in vitro. Then, the molecular mechanisms of ESM1 were further elucidated by bioinformatic end experimental analysis. Results: ESM1 was significantly upregulated in OC and was positively correlated with PFS but negatively correlated with OS. ESM1 knockdown inhibited cell proliferation, apoptosis escape, the cell cycle, angiogenesis, migration and invasion in multiple experiments. Moreover, GSVA found that ESM1 was associated with the Akt pathway, and our results supported this prediction. Conclusion: ESM1 was closely correlated with OC development and progression, and it could be considered a novel biomarker and therapeutic target for OC patients.
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
小婷完成签到,获得积分10
刚刚
可耐的冰萍完成签到,获得积分10
刚刚
shishuang完成签到,获得积分10
刚刚
天桂星完成签到,获得积分10
1秒前
1秒前
充电宝应助小希采纳,获得10
1秒前
vvvvv完成签到,获得积分10
1秒前
圆圆完成签到 ,获得积分10
1秒前
penny发布了新的文献求助10
1秒前
张哈完成签到 ,获得积分10
1秒前
贪玩的寻冬完成签到,获得积分10
3秒前
蓝天发布了新的文献求助20
3秒前
3秒前
酷酷的数据线完成签到,获得积分10
3秒前
3秒前
科研通AI6.2应助小希采纳,获得10
4秒前
许峰发布了新的文献求助10
5秒前
6秒前
科研通AI6.4应助小希采纳,获得10
6秒前
西伯利亚兔完成签到,获得积分10
6秒前
radom完成签到,获得积分10
6秒前
牛牛完成签到,获得积分10
7秒前
传奇3应助洞幺拐采纳,获得10
7秒前
bandian应助Luozhiang采纳,获得10
8秒前
8秒前
ebby完成签到,获得积分10
8秒前
Yy完成签到,获得积分10
8秒前
Tuono完成签到,获得积分10
8秒前
科研通AI6.4应助小希采纳,获得10
9秒前
9秒前
9秒前
七点应助Bruce采纳,获得10
10秒前
FashionBoy应助晴3388采纳,获得10
10秒前
lq8996完成签到,获得积分10
11秒前
11秒前
Will发布了新的文献求助10
11秒前
科研通AI6.4应助小希采纳,获得10
11秒前
ZCX发布了新的文献求助10
12秒前
12秒前
神勇的煎蛋完成签到,获得积分10
12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
Molecular Mechanisms of Photosynthesis, 4th Edition 1000
Organic Reactions, Volume 116 1000
Current concepts in cutaneous toxicity : proceedings of the Fourth Conference on Cutaneous Toxicity, Washington, D.C., May 9-11, 1979 1000
The recovery-stress questionnaires : user manual 800
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 7258067
求助须知:如何正确求助?哪些是违规求助? 8880119
关于积分的说明 18760635
捐赠科研通 6938477
什么是DOI,文献DOI怎么找? 3201248
关于科研通互助平台的介绍 2375276
邀请新用户注册赠送积分活动 2177051