Original Article
Transketolase contributes to hepatocellular carcinoma migration, invasion, angiogenesis, and tumorigenesis
Abstract
Background: Hepatocellular carcinoma (HCC) is the leading cause of cancer death around the world; as the survival of patients with HCC is persistently low, new regulatory factors should be identified to provide new therapeutic targets. The role of the thiamine-dependent enzyme transketolase (TKT) in tumor progression has not been well-studied. In this study, we investigated the role of TKT in HCC progression.
Methods: TKT expression in HCC tissues was analyzed using immunohistochemistry (IHC), and the relationship between TKT level and clinical outcome was examined using the Kaplan–Meier method and the log-rank test. The role of TKT in HCC progression was investigated using the wound healing assay, Transwell assay, chicken chorioallantoic membrane (CAM) assay, soft agar assay, and a xenograft tumor model. Promoter methylation levels in HCC cells and normal LO2 liver cells were examined using bisulfite genomic sequencing.
Results: TKT was upregulated in HCC tissues and cells. Patients with high TKT expression had poor outcome. TKT overexpression promoted HCC migration, invasion, angiogenesis, and tumorigenesis, while TKT knockdown reduced these effects. In addition, we found lower TKT promoter methylation in HCC tissues and cells, indicating that TKT was upregulated in HCC tissues and cells.
Conclusions: Our study demonstrates that TKT is an oncogene in hepatocellular tumorigenesis, and provides a new HCC therapeutic target.
Methods: TKT expression in HCC tissues was analyzed using immunohistochemistry (IHC), and the relationship between TKT level and clinical outcome was examined using the Kaplan–Meier method and the log-rank test. The role of TKT in HCC progression was investigated using the wound healing assay, Transwell assay, chicken chorioallantoic membrane (CAM) assay, soft agar assay, and a xenograft tumor model. Promoter methylation levels in HCC cells and normal LO2 liver cells were examined using bisulfite genomic sequencing.
Results: TKT was upregulated in HCC tissues and cells. Patients with high TKT expression had poor outcome. TKT overexpression promoted HCC migration, invasion, angiogenesis, and tumorigenesis, while TKT knockdown reduced these effects. In addition, we found lower TKT promoter methylation in HCC tissues and cells, indicating that TKT was upregulated in HCC tissues and cells.
Conclusions: Our study demonstrates that TKT is an oncogene in hepatocellular tumorigenesis, and provides a new HCC therapeutic target.
