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Galangin, a Flavonoid from Lesser Galangal, Induced Apoptosis via p53-Dependent Pathway in Ovarian Cancer Cells.

Authors
  • Huang, Haizhi1, 2
  • Chen, Allen Y3
  • Ye, Xingqian4
  • Guan, Rongfa5
  • Rankin, Gary O6
  • Chen, Yi Charlie2
  • 1 College of Life Sciences, China Jiliang University, Hangzhou 310018, China. , (China)
  • 2 College of Science, Technology & Mathematics, Alderson Broaddus University, Philippi, WV 26416, USA.
  • 3 Department of Pharmacy Informatics, Seattle Children's Hospital, Seattle, WA 98101, USA.
  • 4 College of Biosystems Engineering and Food Science, National-Local Joint Engineering Laboratory of Intelligent Food Technology and Equipment, Zhejiang University, Hangzhou 310058, China. , (China)
  • 5 College of Food Science and Engineering, Zhejiang University of Technology, Hangzhou 310014, China. , (China)
  • 6 Department of Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25755, USA.
Type
Published Article
Journal
Molecules
Publisher
MDPI AG
Publication Date
Mar 30, 2020
Volume
25
Issue
7
Identifiers
DOI: 10.3390/molecules25071579
PMID: 32235536
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Among women worldwide, ovarian cancer is one of the most dangerous cancers. Patients undergoing platinum-based chemotherapy might get adverse side effects and develop resistance to drugs. In recent years, natural compounds have aroused growing attention in cancer treatment. Galangin inhibited the growth of two cell lines, A2780/CP70 and OVCAR-3, more strongly than the growth of a normal ovarian cell line, IOSE 364. The IC50 values of galangin on proliferation of A2780/CP70, OVCAR-3 and IOSE 364 cells were 42.3, 34.5, and 131.3 μM, respectively. Flow cytometry analysis indicated that galangin preferentially induced apoptosis in both ovarian cancer cells with respect to normal ovarian cells. Galangin treatment increased the level of cleaved caspase-3 and -7 via the p53-dependent intrinsic apoptotic pathway by up-regulating Bax protein and via the p53-dependent extrinsic apoptotic pathway by up-regulating DR5 protein. By down-regulating the level of p53 with 20 μM pifithrin-α (PFT-α), the apoptotic rates of OVCAR-3 cells induced by galangin treatment (40 μM) were significantly decreased from 18.2% to 10.2%, indicating that p53 is a key regulatory protein in galangin-induced apoptosis in ovarian cancer cells. Although galangin up-regulated the expression of p21, it had little effect on the cell cycle of the two ovarian cancer cell lines. Furthermore, the levels of phosphorylated Akt and phosphorylated p70S6K were decreased through galangin treatment, suggesting that the Akt/p70S6K pathways might be involved in the apoptosis. Our results suggested that galangin is selective against cancer cells and can be used for the treatment of platinum-resistant ovarian cancers in humans.

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