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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.
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