Chuan-Chun Lee1,2, Meng-Liang Lin3, Menghsiao Meng4, Shih-Shun Chen5. 1. Graduate Institute of Biotechnology, National Chung Hsing University, Taichung, Taiwan, R.O.C. 2. Department of Medical Laboratory Science and Biotechnology, Central Taiwan University of Science and Technology, Taichung, Taiwan, R.O.C. 3. Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan, R.O.C. sschen1@ctust.edu.tw mhmeng@dragon.nchu.edu.tw mllinsally@yahoo.com.tw. 4. Graduate Institute of Biotechnology, National Chung Hsing University, Taichung, Taiwan, R.O.C. sschen1@ctust.edu.tw mhmeng@dragon.nchu.edu.tw mllinsally@yahoo.com.tw. 5. Department of Medical Laboratory Science and Biotechnology, Central Taiwan University of Science and Technology, Taichung, Taiwan, R.O.C. sschen1@ctust.edu.tw mhmeng@dragon.nchu.edu.tw mllinsally@yahoo.com.tw.
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. Copyright
BACKGROUND/AIM: Anti-cancer activity of 3,5,7-trihydroxyflavone (galangin) has been documented in a variety of cancer types; however, its effect on humannasopharyngeal 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. Copyright