Anticancer activities of chalcone flavokawain B from Alpinia pricei Hayata in human lung adenocarcinoma (A549) cells via induction of reactive oxygen species-mediated apoptotic and autophagic cell death.

Autor: Hseu YC; Department of Cosmeceutics, College of Biopharmaceutical and Food Sciences, China Medical University, Taichung, Taiwan.; Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan.; Chinese Medicine Research Center, China Medical University, Taichung, Taiwan.; Research Center of Chinese Herbal Medicine, China Medical University, Taichung, Taiwan., Huang YC; Department of Nutrition, College of Biopharmaceutical and Food Sciences, China Medical University, Taichung, Taiwan., Thiyagarajan V; Department of Cosmeceutics, College of Biopharmaceutical and Food Sciences, China Medical University, Taichung, Taiwan., Mathew DC; Department of Cosmeceutics, College of Biopharmaceutical and Food Sciences, China Medical University, Taichung, Taiwan., Lin KY; Department of Medical Research, Chi-Mei Medical Center, Tainan, Taiwan., Chen SC; Department of Life Sciences, National Central University, Chung-Li, Taiwan., Liu JY; Graduate Institute of Cancer Biology, China Medical University, Taichung, Taiwan., Hsu LS; Department of Biomedical Sciences, Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung, Taiwan., Li ML; Department of Nutrition, College of Biopharmaceutical and Food Sciences, China Medical University, Taichung, Taiwan., Yang HL; Department of Nutrition, College of Biopharmaceutical and Food Sciences, China Medical University, Taichung, Taiwan.
Jazyk: angličtina
Zdroj: Journal of cellular physiology [J Cell Physiol] 2019 Aug; Vol. 234 (10), pp. 17514-17526. Date of Electronic Publication: 2019 Mar 07.
DOI: 10.1002/jcp.28375
Abstrakt: Chalcones found in fruits and vegetables have promising cancer chemopreventive properties. This study attempts to identify the anticancer efficacies of chalcone flavokawain B (FKB) in the rhizomes of Alpinia pricei Hayata by examining key molecular events in non-small-cell lung cancer (A549) cells. Our results indicated that in human A549 cells, FKB (0-15 μg/ml) decreases cell viability and colony formation, dysregulates the Bax:B-cell lymphoma 2 ratio and increases apoptotic DNA fragmentation. Mitochondrial (caspase-9/-3 and poly ADP ribose polymerase [PARP]) signaling was found to be involved in FKB-induced apoptosis. In addition, FKB-induced reactive oxygen species (ROS) generation, and N-acetylcysteine attenuated FKB-induced apoptotic cell death. Moreover, FKB triggered autophagy, as evidenced by the improved acidic vesicular organelle formation, lipidated light chain 3 (microtubule-related light chain 3) accumulation, and ATG7 expression and the decreased mammalian target of rapamycin phosphorylation. Furthermore, FKB suppressed ROS-mediated ATG4B expression. Inhibiting autophagy using 3-methyladenine/chloroquine diminished FKB-induced cell death, indicating that autophagy is triggered as a death mechanism by FKB. In summary, FKB has a crucial role in the execution and propagation of ROS-mediated apoptotic and autophagic cell death of lung adenocarcinoma cells.
(© 2019 Wiley Periodicals, Inc.)
Databáze: MEDLINE
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