The expression pattern and clinical implications of TBC1D16 in hepatocellular carcinoma

Hepatocellular carcinoma (HCC), the predominant form of primary liver cancer, demonstrates escalating global incidence and mortality trends. Although emerging evidence suggests that TBC1 domain family member 16 (TBC1D16) significantly contributes to tumorigenesis and malignant progression across multiple cancer types, the relationship between TBC1D16 and HCC remains poorly understood. Our study aims to elucidate the functional role of TBC1D16 in HCC and its potential clinical value.
The expression of TBC1D16 in HCC was analyzed through TCGA and GEO databases, verified via qRT-PCR and Western blotting. Kaplan–Meier survival curves and Cox regression analysis assessed its correlation with HCC prognosis. Cell functional assays explored the impact of TBC1D16 on HCC progression. Potential transcription factors regulating TBC1D16 were identified through transcription factor databases. RNA-seq, KEGG, and GSEA identified TBC1D16-related signaling pathways, which were confirmed by biochemical validation. Finally, TIMER, ssGSEA, TCIA, and GDSC databases were harnessed to predict the impact of immunotherapy and targeted drug therapy.
TBC1D16 expression is higher in HCC tissue than in adjacent normal tissue and is correlated with adverse prognosis of HCC patients. Silencing TBC1D16 reduced the proliferation, migration, and invasion of HCC cells. The expression of TBC1D16 is regulated by SP1.TBC1D16 expression inhibits NF-κB signaling, potentially serving as a mechanism contributing to HCC. Furthermore, TBC1D16 expression also affects immunotherapy responses and drug sensitivity.
TBC1D16 upregulation in HCC is linked to poor prognosis and enhances tumor invasiveness, silencing TBC1D16 activates NF-κB signaling, indicating its potential role in HCC diagnosis.