Amygdalin promotes the activity of T cells to suppress the progression of HBV-related hepatocellular carcinoma via the JAK2/STAT3 signaling pathway

Abstract Background Hepatitis B virus (HBV) infection is a high-risk factor of hepatocellular carcinoma (HCC). Cellular immune responses are essential for HCC development, and the CD4+ CD8+ T subtypes identified as primary anti-tumor cells. In study, we investigated effect mechanism amygdalin in cellular response HBV-related progression. Methods The cell proliferation was examined by MTT analysis. Cells metastasis ability detected Invasion migration assays. Quantification apoptotic cells performed with Flow cytometer assay. protein levels p-STAT3, STAT3, p-JAK2, JAK2, caspase-3, cleaved caspase-3 were performing immunoblotting Results We demonstrate that treatment could rescue HBV-T viability IFN-? TNF-?production. cells, MFI CD8 + lower than NC-T Moreover, phosphorylation STAT3 JAK2 higher compared to those then reduced treatment. Co-culture reduce TNF-?, production while increase IL-6 IL-10 HepG2.2.15 cells; these alterations be partially reversed pretreatment. Finally, co-culture significantly promoted viability, inhibited apoptosis, Conclusion Our findings provide rationale further studies on functions inhibiting proliferation, invasion, via cell-mediated tumor immunity.