研究动态
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Circ_0088300-BOLL相互作用调节线粒体代谢重编程并参与胃癌生长和转移的分子机制。

Molecular Mechanism of Circ_0088300-BOLL Interaction Regulating Mitochondrial Metabolic Reprogramming and Involved in Gastric Cancer Growth and Metastasis.

发表日期:2023 Nov 12
作者: Songtao Chu, Bingyuan Fei, Miao Yu
来源: JOURNAL OF PROTEOME RESEARCH

摘要:

本研究旨在探讨circRNA circ_0088300与RNA结合蛋白(RBP)BOLL相互作用对胃癌生长和转移的影响及分子机制。通过从TCGA数据库中筛选差异表达的RBP基因建立预后风险模型,并确定BOLL为关键RBP。基因集富集分析 (GSEA) 显示 BOLL 与线粒体功能相关。 circ_0088300的上调倍数变化在GSE93541数据集中最高,RPISeq数据库证实了其与BOLL的结合关系。体外实验表明,BOLL调节线粒体代谢和癌细胞功能,并且circ_0088300上调BOLL的表达水平。体内实验表明,敲低circ_0088300可以抑制肿瘤生长和转移,而过表达BOLL可以逆转这种效应。总之,我们得出初步结论,circ_0088300上调BOLL通过促进线粒体代谢重编程促进胃癌生长和转移。
This study aims to investigate the effect and molecular mechanism of the interaction between circRNA circ_0088300 and the RNA binding protein (RBP) BOLL on the growth and metastasis of gastric cancer. A prognostic risk model was established by screening differentially expressed RBP genes from the TCGA database, and BOLL was identified as a critical RBP. Gene Set Enrichment analysis (GSEA) showed that BOLL was associated with mitochondrial function. The upregulation fold change of circ_0088300 was the highest in the GSE93541 data set, and the RPISeq database confirmed its binding relationship with BOLL. In vitro experiments showed that BOLL regulates mitochondrial metabolism and cancer cell function and circ_0088300 upregulates the expression level of BOLL. In vivo experiments demonstrated that knocking down circ_0088300 can inhibit tumor growth and metastasis, whereas overexpression of BOLL can reverse this effect. In conclusion, we have reached a preliminary conclusion that upregulation of BOLL by circ_0088300 promotes gastric cancer growth and metastasis by promoting mitochondrial metabolic reprogramming.