Role of arbutin in the inhibition of FBXO5 in hepatocellular carcinoma.

IF 2.8 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Shuo Zhang, Kai Yao, Yangjing Pi, Sen Yang, Zheng Huang, Xueshan Pan, Tonggang Li
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引用次数: 0

Abstract

Purpose: This work investigated the effect of FBXO5 in hepatocellular carcinoma (HCC) and the mechanism of action of arbutin in its inhibition.

Methods: FBXO5 mRNA and protein expressions in the tumor were assessed using TCGA, ICGC and HPA databases. Cox regression analysis and Kaplan-Meier survival curves were employed to assess the impact of FBXO5 on the survival outcomes of patients with HCC. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Set Enrichment Analysis (GSEA), and Gene Set Variation Analysis (GSVA) were used to investigate the biological function associated with FBXO5-related genes. The role of FBXO5 as oncogene and the inhibitory mechanism of arbutin were confirmed through western blotting (WB), reverse transcription quantitative polymerase chain reaction (RT-qPCR), and in vitro experiments such as scratch wound-healing migration assay, plate clone formation assay, and transwell migration assay.

Results: Patients with high FBXO5 expression showed shorted overall survival (OS), progression-free survival (PFS), disease-specific survival (DSS), and disease-free survival (DFS). FBXO5 was identified as an independent prognostic risk factor associated with the cell cycle. In vitro investigations indicated that FBXO5 facilitated HCC progression by modulating the cell cycle, while arbutin suppressed FBXO5 expression and regulated cell cycle dynamics.

Conclusion: FBXO5 is a potential diagnostic and prognostic biomarker for HCC, and arbutin may exert anticancer effects through the suppression of FBXO5 expression.

熊果苷在肝癌中抑制FBXO5的作用。
目的:探讨FBXO5在肝细胞癌(HCC)中的作用及熊果苷抑制其作用的机制。方法:采用TCGA、ICGC和HPA数据库检测FBXO5 mRNA和蛋白在肿瘤中的表达。采用Cox回归分析和Kaplan-Meier生存曲线评估FBXO5对HCC患者生存结局的影响。利用基因本体(GO)、京都基因与基因组百科全书(KEGG)、基因集富集分析(GSEA)和基因集变异分析(GSVA)对fbxo5相关基因的生物学功能进行研究。通过western blotting (WB)、逆转录定量聚合酶链反应(RT-qPCR)及抓伤愈合迁移实验、平板克隆形成实验、transwell迁移实验等体外实验,证实FBXO5作为致癌基因的作用及熊果苷的抑制机制。结果:FBXO5高表达患者总生存期(OS)、无进展生存期(PFS)、疾病特异性生存期(DSS)和无病生存期(DFS)均较短。FBXO5被确定为与细胞周期相关的独立预后危险因素。体外研究表明,FBXO5通过调节细胞周期促进HCC的进展,而熊果苷抑制FBXO5的表达,调节细胞周期动力学。结论:FBXO5是HCC的潜在诊断和预后生物标志物,熊果苷可能通过抑制FBXO5的表达发挥抗癌作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Discover. Oncology
Discover. Oncology Medicine-Endocrinology, Diabetes and Metabolism
CiteScore
2.40
自引率
9.10%
发文量
122
审稿时长
5 weeks
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