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Molecules 2019, 24(4), 673; https://doi.org/10.3390/molecules24040673

Theaflavin-3,3′-Digallate Suppresses Human Ovarian Carcinoma OVCAR-3 Cells by Regulating the Checkpoint Kinase 2 and p27 kip1 Pathways

1
Tea Research Institute Chinese Academy of Agricultural Sciences, Ministry of Agriculture, Hangzhou 310008, China
2
Department of Tea Science, Zhejiang University, Hangzhou 310058, China
3
College of Science, Technology and Mathematics, Alderson Broaddus University, Philippi, WV 26416, USA
*
Authors to whom correspondence should be addressed.
Received: 23 January 2019 / Revised: 9 February 2019 / Accepted: 12 February 2019 / Published: 14 February 2019
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Abstract

Theaflavin-3,3′-digallate (TF3) is a unique polyphenol in black tea. Epidemiological studies have proved that black tea consumption decreases the incidence rate of ovarian cancer. Our former research demonstrated that TF3 inhibited human ovarian cancer cells. Nevertheless, the roles of checkpoint kinase 2 (Chk2) and p27 kip1 (p27) in TF3-mediated inhibition of human ovarian cancer cells have not yet been investigated. In the current study, TF3 enhanced the phosphorylation of Chk2 to modulate the ratio of pro/anti-apoptotic Bcl-2 family proteins to initiate intrinsic apoptosis in a p53-independent manner and increased the expression of death receptors to activate extrinsic apoptosis in OVCAR-3 human ovarian carcinoma cells. In addition, TF3 up-regulated the expression of p27 to induce G0/G1 cell cycle arrest in OVCAR-3 cells. Our study indicated that Chk2 and p27 were vital anticancer targets of TF3 and provided more evidence that TF3 might be a potent agent to be applied as adjuvant treatment for ovarian cancer. View Full-Text
Keywords: theaflavin-3,3′-digallate; apoptosis; death receptors; Chk2; cell cycle arrest; p27 theaflavin-3,3′-digallate; apoptosis; death receptors; Chk2; cell cycle arrest; p27
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Gao, Y.; Yin, J.; Tu, Y.; Chen, Y.C. Theaflavin-3,3′-Digallate Suppresses Human Ovarian Carcinoma OVCAR-3 Cells by Regulating the Checkpoint Kinase 2 and p27 kip1 Pathways. Molecules 2019, 24, 673.

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