Dihydromyricetin promotes apoptosis, suppresses proliferation and tumor necrosis factor-α-mediated nuclear factor kappa-B activation in nasopharyngeal carcinoma CNE-2 cell

Objective To investigate the efficacy of dihydromyricetin (DMY) on nasopharyngeal carcinoma (NPC) cell proliferation, apoptosis and to reveal the underlying mechanism in vitro experiments. Methods The CNE-2 cell line was treated with different concentrations of DMY and the effects of DMY on cell viability and proliferation were evaluated using cell counting kit-8 (CCK-8) assay and plate colony formation assay. Cellular apoptosis was detected by flow cytometry following Annexin V fluorescein isothiocyanate/propidine iodide staining. Nuclei morphology was observed under a fluorescence microscope following Hoechst 333258 staining. The expression of phosphorylated inhibitor of nuclear factor kappa-B kinase subunit beta (p-IKKβ), phosphorylated inhibitor of nuclear factor kappa-B kinase subunit alpha (p-IKKα), inhibitor of nuclear factor kappa-B alpha (IκB-α), nuclear factor kappa-B (NF-κB)/p65 was examined by Western blot analysis and the nuclear translocation of NF-κB/p65 was observed using a confocal laser scanning microscopy. Results DMY inhibited the proliferative capability and colony formation of NPC CNE-2 cells. Meanwhile, DMY induced apoptosis of CNE-2 cells in a dose and time-dependent manner via upregulating B-cell lymphoma-2 associated X, but downregulating B-cell lymphoma-2 and pro-caspase-3. Importantly, we found that DMY suppressed tumor necrosis factor alpha (TNF-α)-mediated NF-κB activation via inhibiting p-IKKβ, p-IKKα and blocking NF-κB subunit p65. Conclusion Our experiments demonstrated that DMY had significant antiproliferative and apoptosisinducing effects on CNE-2 cells. Additionally, DMY promoted inactivation of p-IKKβ, p-IKKα, and blocked the nuclear translocation of NF-κB subunit p65. These results suggest that DMY may be an important therapeutic approach for NPC.