APOF regulates the malignancy and inflammatory response of hepatocellular carcinoma cells through PPAR signaling pathway

This is the authors' abstract. We don't add key points for this paper.

Hepatocellular carcinoma (HCC) is a malignant tumor with high incidence. It is often diagnosed at an advanced stage, with intrahepatic or extrahepatic metastasis, and cannot be cured by radical surgery. In human HCC cell lines, Apolipoprotein F (APOF) gene promoter activity was significantly increased, but the relationship between the two has not been elucidated. This study aims to investigate the mechanism by which Apolipoprotein F (APOF), one of the key proteins in the regulation of lipid metabolism, affects the malignancy and inflammatory response of HCC. RNA was measured via RT-qPCR, protein was detected with Western blot. Cell viability aand proliferation were assessed using CCK8 assay, colony formation and EdU assays. Tunel assay measure cell apoptosis. Inflammatory cytokines were measured with ELISA kits. APOF reduced in HCC tissues and cells notably. LPS reduced APOF in HCC cells, increased the viability, proliferation and inflammatory response of HCC cells, and reduced apoptosis. Overexpression of APOF increased PPARα and PPARγ, while reducing the malignant and inflammatory response of HCC cells by regulating PPAR signaling pathway. We found a decrease of APOF in HCC patients, and confirmed that increasing APOF expression can inhibit tumor development and inflammatory response via PPAR signaling pathway, providing a potential direction for clinical treatment of HCC.