Profiling and Characterization of microRNAs Responding to Sodium Butyrate Treatment in Gastric Cancer Cells

丁酸钠 小RNA 丁酸盐 癌症研究 细胞凋亡 小桶 癌症 生物 化学 分子生物学 癌细胞 计算生物学 细胞生物学 生物化学 细胞 基因 基因表达 转录组 遗传学 发酵
作者
Dewei Zhang,Gongping Sun,He Duan,Jin Meng
出处
期刊:Combinatorial Chemistry & High Throughput Screening [Bentham Science Publishers]
卷期号:25 (11): 1875-1888 被引量:4
标识
DOI:10.2174/1386207325666211027154207
摘要

Short-chain fatty acids exert anti-cancer effects on tumor cells.We aimed to reveal the signaling network altered by butyrate in Gastric Cancer (GC) using small RNA sequencing (sRNA-seq).The effects of butyrate on the biological behavior of NCI-N87 and KATO III cells in vitro were assessed by functional assays and half-maximal inhibitory concentrations (IC50) of butyrate in KATO III cells were calculated. sRNA-seq was performed on KATO III cells. Differentially expressed miRNAs (DE-miRNAs) were identified between butyrate treatment and control groups using DESeq2, and miRNA targets were predicted. A protein-protein interaction (PPI) network of DE-miRNA targets was created using Metascape. Key MCODE complexes were identified using the MCODE algorithm and cluster Profiler. The relationship between DE-miRNA and GC overall survival (OS) was evaluated using Kaplan-Meier curves.Butyrate dose-dependently inhibited NCI-N87 and KATO III cell viability. KATO III cells were more sensitive to butyrate than NCI-N87 cells. Butyrate promoted apoptosis and inhibited KATO III cell migration. Total 324 DE-miRNAs were identified in KATO III cells, and 459 mRNAs were predicted as targets of 83 DE-miRNAs. Two key protein complexes were identified in a PPI network of the 459 targets. A key signaling network responding to butyrate was generated using targets in these key complexes and their miRNA regulators. The DE-miRNAs in the key signaling network were related to the OS of GC.Butyrate altered the biological behavior of GC cells, which may be achieved by regulating miRNAs and related oncogenic pathways.
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
2秒前
奋斗的妙海完成签到 ,获得积分10
3秒前
HHEHK完成签到 ,获得积分10
5秒前
胡晓龙发布了新的文献求助10
5秒前
新的旅程完成签到,获得积分10
7秒前
完犊子发布了新的文献求助10
8秒前
木康薛完成签到,获得积分10
9秒前
地德兴完成签到 ,获得积分10
9秒前
10秒前
339564965完成签到,获得积分10
11秒前
安静严青完成签到 ,获得积分10
11秒前
12秒前
柏林寒冬应助完犊子采纳,获得10
13秒前
ccc完成签到,获得积分10
13秒前
TianFuAI完成签到,获得积分10
14秒前
chee完成签到,获得积分10
15秒前
研友_ZA2B68完成签到,获得积分0
15秒前
inu1255完成签到,获得积分0
15秒前
只想顺利毕业的科研狗完成签到,获得积分10
16秒前
普鲁卡因发布了新的文献求助10
17秒前
Helios完成签到,获得积分10
18秒前
xueshidaheng完成签到,获得积分0
18秒前
BK_201完成签到,获得积分10
18秒前
风信子完成签到,获得积分10
19秒前
abiorz完成签到,获得积分0
19秒前
窗外是蔚蓝色完成签到,获得积分0
20秒前
nanostu完成签到,获得积分10
22秒前
吐司炸弹完成签到,获得积分10
22秒前
mayfly完成签到,获得积分10
23秒前
Brief完成签到,获得积分10
23秒前
大模型应助科研通管家采纳,获得10
24秒前
小二郎应助科研通管家采纳,获得10
24秒前
24秒前
科研通AI2S应助科研通管家采纳,获得10
24秒前
Amikacin完成签到,获得积分10
24秒前
鹏举瞰冷雨完成签到,获得积分10
24秒前
整齐的惮完成签到 ,获得积分10
25秒前
1122完成签到 ,获得积分10
25秒前
情怀应助Cheung2121采纳,获得30
27秒前
完犊子完成签到,获得积分20
27秒前
高分求助中
【提示信息,请勿应助】关于scihub 10000
Les Mantodea de Guyane: Insecta, Polyneoptera [The Mantids of French Guiana] 3000
徐淮辽南地区新元古代叠层石及生物地层 3000
The Mother of All Tableaux: Order, Equivalence, and Geometry in the Large-scale Structure of Optimality Theory 3000
Handbook of Industrial Diamonds.Vol2 1100
Global Eyelash Assessment scale (GEA) 1000
Picture Books with Same-sex Parented Families: Unintentional Censorship 550
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 4038112
求助须知:如何正确求助?哪些是违规求助? 3575788
关于积分的说明 11373801
捐赠科研通 3305604
什么是DOI,文献DOI怎么找? 1819255
邀请新用户注册赠送积分活动 892655
科研通“疑难数据库(出版商)”最低求助积分说明 815022