DTYMK promote hepatocellular carcinoma proliferation by regulating cell cycle

Area of Science:

• Oncology
• Molecular Biology
• Genetics

Background:

• Overexpression of DTYMK is implicated in tumorigenesis and progression across various human cancers.
• The specific role of DTYMK in hepatocellular carcinoma (HCC) remains largely undefined.
• Understanding DTYMK's function in HCC is crucial for developing targeted therapies.

Purpose of the Study:

• To investigate the expression levels of DTYMK in HCC tumors and adjacent tissues.
• To analyze the correlation between DTYMK expression and patient prognosis in HCC.
• To elucidate the functional role of DTYMK in HCC cell proliferation and cell cycle regulation.

Main Methods:

• DTYMK expression analysis in HCC cohorts (GEO, TCGA, ICGC).
• Survival analysis (Overall Survival, Relapse-Free Survival, Disease-Specific Survival) using Kaplan-Meier.
• In vitro studies involving DTYMK knockdown and overexpression in HCC cell lines to assess proliferation and cell cycle effects.

Main Results:

• DTYMK was significantly upregulated in HCC tumor tissues compared to adjacent liver tissues across multiple datasets.
• High DTYMK expression was strongly associated with poorer overall survival (OS), relapse-free survival (RFS), and disease-specific survival (DSS) in HCC patients.
• Knockdown of DTYMK inhibited HCC cell proliferation by interfering with the cell cycle, while DTYMK overexpression promoted proliferation.

Conclusions:

• DTYMK is a significantly upregulated gene in hepatocellular carcinoma.
• Elevated DTYMK expression serves as a marker for poor prognosis in HCC patients.
• DTYMK promotes HCC tumor growth and proliferation, likely by influencing the cell cycle, suggesting it as a potential therapeutic target.