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pmid:34369850
DTYMK promote hepatocellular carcinoma proliferation by regulating cell cycle.
Tianhao Zhou · Rui Qin · Susu Shi · Hua Zhang · Chuanling Niu · Gaoda Ju · Sen Miao
Cell cycle (Georgetown, Tex.) · 2021 doi:10.1080/15384101.2021.1958502
Paper
complete
Experiment
complete
Data
partial
Analysis
complete
Execution
absent
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Complete file
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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 (RFS) and disease-specific survival (DSS) (all P < 0.05). In conclusion, DTYMK is upregulated in tumors and correlated with poor prognosis in HCC patients. In our report, DTYMK is higher expression in HCC cancer tissue and cell line than tumor adjacent tissue and normal liver cell line. 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