Integrated bioinformatics analysis reveals significant genes associated with cryptorchidism (CO)

基因 生物 古伯纳库姆 基因本体论 基因调控网络 细胞外基质 折叠变化 遗传学 生物信息学 计算生物学 基因表达 内分泌学
作者
Liren Hu,Xianming Fan,Jianfeng Lin,Fulv Liang,Jianping Tu,Zhaojian Guo
出处
期刊:Research Square - Research Square
标识
DOI:10.21203/rs.3.rs-1690590/v1
摘要

Abstract Objective: we performed a comprehensive bioinformatics analysis to identify potential genes and signaling pathways associated with cryptorchidism. Materials and Methods: This study aimed to identify genes significantly associated with cryptorchidism (CO), between the LE and ORL gubernaculum groups at GD17 and GD19 stages, using a GSE57924 dataset. We identified other DEGs which were changed to up-regulation or down-regulation between the groups by adjusting the cut-off (|log2 fold change (FC)| ≥0.5 and adjusted p <0.05). We subjected the identified DEGs to gene ontology (GO) and pathway enrichment analyses, using an online database DAVID, then employed Cytoscape v3.7.1 to construct a protein-protein interaction network. Results: We detected functional hub genes using MCODE. Overall, we identified 147 DEGs between the LE gubernaculum group and ORL gubernaculum group, of which 33 genes were up-regulated (21 genes always down-regulated and 13 genes from down-regulated in GD17 to up-regulated in GD19) while 96 was down-regulated (27 genes always down-regulated and 69 genes from up-regulated in GD17 to down-regulated in GD19). Gene Ontology (GO) revealed that cell adhesion and extracellular matrix were the most abundant biological processes and Cellular Components, whereas the ECM-receptor interaction was the most significant pathway. Analysis of hub genes in the PPI network revealed that 7 genes including Igfbp5, Cyr61, Lamb1, Lamc1, Cp, Fn1, and Ltbp1, were significantly associated with CO. Conclusions: we successfully identified 7 significant markers that provide valuable insights into the molecular mechanism of cryptorchidism. Of note, one of the genes (Fn1) was verified significant differential expression gene in human testicular cancer.

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
hahaha2完成签到,获得积分10
刚刚
MaxwellZH完成签到,获得积分10
刚刚
Ava应助宝贝888888采纳,获得10
1秒前
sheep完成签到,获得积分10
1秒前
maybe完成签到,获得积分10
1秒前
James完成签到,获得积分10
1秒前
simon666完成签到,获得积分10
1秒前
syltharion完成签到,获得积分10
1秒前
yc完成签到,获得积分10
2秒前
Paff完成签到,获得积分10
2秒前
2秒前
Tom2077完成签到,获得积分10
2秒前
2秒前
徐彬荣完成签到,获得积分10
3秒前
LGA1700完成签到,获得积分10
3秒前
清风徐来完成签到,获得积分10
3秒前
Walton完成签到,获得积分10
4秒前
hahaha1完成签到,获得积分10
4秒前
量子咸鱼K完成签到,获得积分10
4秒前
qqqdewq完成签到,获得积分10
4秒前
PaperCrane完成签到,获得积分10
4秒前
surlamper完成签到,获得积分10
5秒前
fate完成签到,获得积分10
5秒前
霡霂完成签到,获得积分10
5秒前
执着柏柳完成签到,获得积分10
5秒前
星辰大海应助科研通管家采纳,获得10
5秒前
1024504036发布了新的文献求助10
6秒前
Likz完成签到,获得积分10
8秒前
Daria完成签到 ,获得积分10
8秒前
科研通AI6.4应助WEileen采纳,获得10
9秒前
栀蓝完成签到 ,获得积分10
20秒前
缓慢的甜瓜完成签到,获得积分10
30秒前
龙猫爱看书完成签到,获得积分10
36秒前
AllRightReserved应助宝贝888888采纳,获得10
43秒前
xuxu213发布了新的文献求助10
45秒前
谦让的映容完成签到,获得积分10
48秒前
yin完成签到,获得积分10
49秒前
科研通AI6.1应助湖里采纳,获得10
52秒前
goodsheperd完成签到 ,获得积分10
54秒前
等待的幼晴完成签到,获得积分10
58秒前
高分求助中
Signals, Systems, and Signal Processing 610
Annie Ernaux: De la perte au corps glorieux 600
Petrology and Plate Tectonics,2025 500
Direct and Iterative Linear System Solvers 400
Cardiopulmonary Bypass and Mechanical Support: Principles and Practice, Fifth Edition 400
Circular Polar Constellations Providing Continuous Single or Multiple Coverage Above a Specified Latitude 400
Burger's Medicinal Chemistry and Drug Discovery 400
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 6758934
求助须知:如何正确求助?哪些是违规求助? 8486103
关于积分的说明 18089041
捐赠科研通 6042414
什么是DOI,文献DOI怎么找? 3009824
邀请新用户注册赠送积分活动 1986656
关于科研通互助平台的介绍 1959732