DTYMK promote hepatocellular carcinoma proliferation by regulating cell cycle.

ABSTRACT: Overexpression of DTYMK is related with tumorigenesis and progression in several human tumors. However, the role of upregulated DTYMK in hepatocellular carcinoma (HCC) patients still remains unclear. In this study, the DTYMK expression in HCC tumors was evaluated in three GEO series (GSE14520, GSE54236, GSE63898), TCGA-LIHC, and ICGC-IRLR-JP cohorts. Survival analysis of DTYMK based on TCGA-LIHC and ICGC-LIRI-JP cohorts was conducted. We found that DTYMK was dramatically upregulated in tumor tissue compared with that in adjacent liver tissue. Kaplan-Meier analysis revealed that high expression of DTYMK in HCC patients' tumor tissue was significantly corresponded to worse overall survival (OS) (P < 0.05). Further analysis showed that overexpressing DTYMK led to poor relapse free survival (R

SUBMITTER: Zhou T 

PROVIDER: S-EPMC8489954 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature