The immunoglobulin superfamily member 3 (IGSF3) promotes hepatocellular carcinoma progression through activation of the NF-κB pathway.

BACKGROUND

Patients with hepatocellular carcinoma (HCC) suffer from a high fatality rate, likely due to increased incidence of tumor relapse and metastasis. Understanding the molecular mechanisms that contribute to HCC development and progression is vital for the discovery of new treatment targets. This study aims to explore the expression profiles and functions of immunoglobulin superfamily member 3 (IGSF3) in HCC.

METHODS

We evaluated IGSF3 levels in HCC and normal tissues using bioinformatics, western blot, quantitative real-time PCR (qRT-PCR), and immunohistochemistry. We also conducted proliferation assays, colony formation assays, flow cytometry, cell migration assay, cell invasion assay, qRT-PCR, and western blotting in HCC cell lines. Immunofluorescence and western blotting further used to study the IGSF3 pathway. A mouse xenograft model was utilized to examine the influence of IGSF3 on HCC growth .

RESULTS

IGSF3 levels were higher in HCC tissues and cell lines. Silencing of IGSF3 via lentiviral vector system (LV) inhibited migration, invasion, and growth of HCC cell lines as well as tumor growth . Overexpression of IGSF3 promoted result . Importantly, we found that IGSF3 activates the NF-κB pathway to promote tumorigenic features in HCC cell lines.

CONCLUSIONS

We found that IGSF3 can be used as a novel biomarker for HCC detection. Moreover, IGSF3 elicits HCC progression by activating the NF-κB pathway. As such, our data provides potential options for therapeutic targets in patients with HCC.