Galangin Induces p53-independent S-phase Arrest and Apoptosis in Human Nasopharyngeal Carcinoma Cells Through Inhibiting PI3K-AKT Signaling Pathway.

BACKGROUND/AIM: Anti-cancer activity of 3,5,7-trihydroxyflavone (galangin) has been documented in a variety of cancer types; however, its effect on human nasopharyngeal carcinoma (NPC) cells remains undetermined.

MATERIALS AND METHODS: Human NPC cell lines were treated with galangin. Apoptosis was analyzed by assessing nuclear condensation, cleavage of pro-caspase-3 and poly ADP-ribose polymerase (PARP), and DNA fragmentation. Short hairpin RNA-mediated silencing of p53 was used for characterizing the role of p53 in the anti-cancer activity of galangin. Phosphatidylinositol 3-kinase (PI3K) inhibitor, protein kinase B (AKT) inhibitor, and ectopic expression of wild type p85α or p85α mutant lacking p110α-binding ability were utilized to confirm the involvement of PI3K/AKT inactivation in galangin-induced apoptosis.

RESULTS: Galangin induces apoptosis and S-phase arrest by attenuating the PI3K/AKT signaling pathway. Silencing of p53 did not block the anti-cancer activity of galangin on NPC cells.

CONCLUSION: Galangin effects on apoptosis and S-phase arrest in NPC cells are mediated via interfering with the PI3K-AKT signaling pathway in a p53-independent manner.