inhibits the malignant progression of hepatocellular carcinoma by inhibiting expression and epithelial-mesenchymal transition.

BACKGROUND

Hepatocellular carcinoma (HCC) is a prevalent liver malignancy. This study examined the roles of transforming growth factor beta () and cytochrome b5 domain containing 2 () in HCC etiology and their prognostic biomarker potential.

METHODS

Key modules and prognostic genes were identified by analyzing the GSE101685 dataset by weighted gene co-expression network analysis (WGCNA) and Least absolute shrinkage and selection operator (LASSO) Cox regression. The expression levels of and in HCC cell lines were quantified using Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting (WB) assays. Effects of overexpression on cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) marker regulation were assessed , while tumorigenicity was evaluated using a xenograft model of HCC in nude mice.

RESULTS

In this study, WGCNA identified the turquoise module as significantly associated with HCC, containing 452 DEGs. LASSO Cox regression analysis revealed 9 key prognostic genes, with being underexpressed in HCC cells and tissues. was negatively correlated with expression, resulting in poor patient prognosis. Functional assays demonstrated that overexpression inhibited proliferation, migration, and invasion of HCC cell lines, and altered EMT marker expression. Furthermore, the addition of partially reversed the suppressive effects caused by overexpression. , CYB5D2 overexpression significantly reduced tumor growth, indicating its potential as a therapeutic target for HCC.

CONCLUSION

The tumor suppressor function of in HCC and its interaction with offered fresh information on the molecular pathophysiology of HCC and possible treatment avenues.