SMYD5 acts as a potential biomarker for hepatocellular carcinoma

Determining the prognosis of patients remains a challenge due to the phenotypic and molecular diversities of hepatocellular carcinomas (HCC). We aimed to evaluate the role of SMYD5 in HCC. Wilcoxon signed-rank test and logistic regression analyzed the relationship between clinical pathologic features and SMYD5. We found that increased expression of SMYD5 in HCC was closely associated with high histologic grade, stage, T stage and nodal stage. Kaplan-Meier method, Cox regression, univariate analysis and multivariate analysis detected overall survival of TCGA-HCC patients. It turned out that high expression of SMYD5 predicted a worse prognosis in HCC. Gene Set Enrichment Analysis (GSEA) was applied via TCGA data set, which indicated that complement and coagulation cascades, fatty acid metabolism, primary bile acid biosynthesis, drug metabolism cytochrome P450, PPAR signaling pathway and retinol metabolism were differentially enriched in SMYD5 high expression phenotype. Interestingly, we proved that SMYD5 upregulation in HCC cells was induced by promoter hypomethylation. Moreover, functional experiments demonstrated that SMYD5 silencing abrogated cell proliferation, migration and invasion and enhanced paclitaxel sensitivity in HCC. All findings implied that SMYD5 might be an underlying biomarker for prognosis and treatment of HCC.

Automated summary

This study aimed to evaluate the role of SMYD5 in hepatocellular carcinomas (HCC). The results showed that high expression of SMYD5 was associated with worse prognosis in HCC patients. Further analysis revealed that SMYD5 upregulation in HCC cells was induced by promoter hypomethylation, and silencing SMYD5 inhibited cell proliferation, migration, invasion, and enhanced sensitivity to paclitaxel.