DBF4B promotes hepatocellular carcinoma progression by regulating CCNA2 and PSMD11 expression

Area of Science:

• Oncology
• Molecular Biology
• Cancer Research

Background:

• Hepatocellular carcinoma (HCC) is an aggressive malignancy with poor outcomes.
• Novel biomarkers and therapeutic targets are crucial for improving HCC management.
• The role of DBF4 zinc finger B (DBF4B) in HCC is not well understood.

Purpose of the Study:

• To investigate the role of DBF4B in HCC progression.
• To evaluate DBF4B as a prognostic biomarker and therapeutic target for HCC.

Main Methods:

• Analyzed DBF4B expression in HCC tissues and cell lines using GEO and TCGA databases.
• Performed survival analysis, nomogram construction, and tissue microarray validation.
• Conducted in vitro functional experiments (cell proliferation, migration, rescue assays) and in vivo xenograft models.
• Explored downstream mechanisms using bioinformatics, qRT-PCR, and Western blotting.

Main Results:

• DBF4B expression is upregulated in HCC and associated with shorter overall and progression-free survival.
• DBF4B silencing suppressed HCC cell proliferation and migration.
• DBF4B promotes cell cycle progression by regulating CCNA2 and PSMD11.
• DBF4B silencing inhibited tumor growth in vivo.

Conclusions:

• DBF4B acts as an oncogene in HCC, promoting proliferation and migration.
• DBF4B is a potential prognostic biomarker and therapeutic target for HCC.