Comprehensive expression analysis reveals several miRNAs against acute pancreatitis via modulating autophagy

小RNA 自噬 生物 PI3K/AKT/mTOR通路 信号转导 细胞生物学 蛋白激酶B 癌症研究 遗传学 基因 细胞凋亡
作者
Xiaoju Su,Fanyang Kong,Qichen Zhang,Mengni Jiang,Lei Wang,Xiangyu Kong,Yiqi Du
出处
期刊:Cellular and Molecular Biology 卷期号:69 (3): 129-134 被引量:3
标识
DOI:10.14715/cmb/2023.69.3.18
摘要

Acute pancreatitis (AP) had been one of the main reasons for hospitalization worldwide. However, the mechanisms related to AP remained to be unclear. This study identified 37 miRNAs and 189 mRNAs were differentially expressed in pancreatitis and normal samples. Bioinformatics analysis showed DEGs were significantly related to PI3K-Akt signaling, FoxO signaling, Oocyte meiosis, Focal adhesion, and Protein digestion and absorption. By constructing a signaling-DEGs regulation network, we found COL12A1, DPP4, COL5A1, COL5A2, and SLC1A5 were related to regulating Protein digestion and absorption, THBS2, BCL2, NGPT1, EREG, COL1A1 were related to regulating PI3K signaling, CCNB1, CDKN2B, IRS2, PLK2 were related to modulating FOXO signaling. Next, we constructed 1 miRNA-mRNA regulation network in AP, consisting of 34 miRNAs and 96 mRNAs. The protein-protein interaction networks and the miRNA-targets networks analysis show that hsa-miR-199a-5p, hsa-miR-150, hsa-miR-194, COL6A3 and CNN1 acted as hub regulators in AOf note, through comprehensive expression analysis, we found several miRNAs and mRNAs were significantly related to modulating autophagy signaling in AP, including hsa-miR-181c, hsa-miR-181d, hsa-miR-181b, hsa-miR-379 and hsa-miR-199a-5Overall, this study screening differently expressed miRNAs in AP and revealed miRNA- autophagy regulation may serve as a potential prognosis and Therapeutic marker for AP.
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
华仔应助进取拼搏采纳,获得10
刚刚
1秒前
dingdong发布了新的文献求助10
1秒前
you完成签到 ,获得积分10
2秒前
qwf完成签到 ,获得积分10
2秒前
3秒前
万能图书馆应助一一采纳,获得10
3秒前
执着跳跳糖完成签到 ,获得积分10
4秒前
阳yang完成签到,获得积分10
4秒前
牛头人完成签到,获得积分10
4秒前
5秒前
Rrr发布了新的文献求助10
5秒前
6秒前
6秒前
serenity完成签到 ,获得积分10
6秒前
Benliu完成签到,获得积分10
6秒前
csq发布了新的文献求助10
7秒前
8秒前
Hello应助外向的醉易采纳,获得10
8秒前
DWWWDAADAD完成签到,获得积分10
11秒前
科研通AI5应助一天八杯水采纳,获得10
12秒前
杨大仙儿完成签到 ,获得积分10
12秒前
14秒前
坚强的广山应助木头人采纳,获得200
14秒前
嘻哈学习完成签到,获得积分10
14秒前
14秒前
14秒前
ying完成签到,获得积分10
15秒前
15秒前
虚幻白玉完成签到,获得积分10
16秒前
安静的孤萍完成签到,获得积分10
17秒前
17秒前
lyz666发布了新的文献求助10
17秒前
liuxl发布了新的文献求助10
18秒前
smile完成签到,获得积分20
19秒前
Shuo Yang完成签到,获得积分10
19秒前
19秒前
伊酒发布了新的文献求助10
19秒前
蓉儿完成签到 ,获得积分10
20秒前
高分求助中
Continuum Thermodynamics and Material Modelling 3000
Production Logging: Theoretical and Interpretive Elements 2700
Social media impact on athlete mental health: #RealityCheck 1020
Ensartinib (Ensacove) for Non-Small Cell Lung Cancer 1000
Unseen Mendieta: The Unpublished Works of Ana Mendieta 1000
Bacterial collagenases and their clinical applications 800
El viaje de una vida: Memorias de María Lecea 800
热门求助领域 (近24小时)
化学 材料科学 生物 医学 工程类 有机化学 生物化学 物理 纳米技术 计算机科学 内科学 化学工程 复合材料 基因 遗传学 物理化学 催化作用 量子力学 光电子学 冶金
热门帖子
关注 科研通微信公众号,转发送积分 3527961
求助须知:如何正确求助?哪些是违规求助? 3108159
关于积分的说明 9287825
捐赠科研通 2805882
什么是DOI,文献DOI怎么找? 1540070
邀请新用户注册赠送积分活动 716926
科研通“疑难数据库(出版商)”最低求助积分说明 709808