1. Galangin Induces p53-independent S-phase Arrest and Apoptosis in Human Nasopharyngeal Carcinoma Cells Through Inhibiting PI3K-AKT Signaling Pathway
- Author
-
Meng Liang Lin, Shih-Shun Chen, Menghsiao Meng, and Chuan-Chun Lee
- Subjects
0301 basic medicine ,Cancer Research ,Cell Survival ,Apoptosis ,Cell Line ,03 medical and health sciences ,chemistry.chemical_compound ,Phosphatidylinositol 3-Kinases ,0302 clinical medicine ,Cell Line, Tumor ,medicine ,Humans ,Protein kinase B ,PI3K/AKT/mTOR pathway ,Flavonoids ,Akt/PKB signaling pathway ,Caspase 3 ,Nasopharyngeal Neoplasms ,General Medicine ,medicine.disease ,Galangin ,030104 developmental biology ,Oncology ,chemistry ,Nasopharyngeal carcinoma ,030220 oncology & carcinogenesis ,S Phase Cell Cycle Checkpoints ,Cancer research ,DNA fragmentation ,RNA Interference ,Signal transduction ,Poly(ADP-ribose) Polymerases ,Tumor Suppressor Protein p53 ,Proto-Oncogene Proteins c-akt ,Signal Transduction - Abstract
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.
- Published
- 2017