Apoptotic Effect of Sanggenol L via Caspase Activation and Inhibition of NF‐κB Signaling in Ovarian Cancer Cells |
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Authors: | Kyeong‐Hwa Seo Bo‐Im Kim Ju‐Ha Kim Jung Hyo Kim Bonglee Kim Nam‐In Baek Sung‐Hoon Kim |
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Affiliation: | 1. Department of Oriental Medicine Biotechnology, Graduate School of Biotechnology, Kyung Hee University, Yongin, Korea;2. College of Korean Medicine, Kyung Hee University, Seoul, Korea;3. Chosun Nursing College, Gwangju, Korea |
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Abstract: | In the present study, the underlying apoptotic mechanism of sanggenol L was elucidated in ovarian cancer cells. Sanggenol L showed cytotoxic and antiproliferative effect in A2780, SKOV‐3, and OVCAR‐3 ovarian cancer cells in a concentration‐dependent fashion. Consistently, sanggenol L increased sub‐G1 phase population and early and late apoptotic portion in ovarian cancer cells. Also, sanggenol L activated caspase9/3, suppressed the phosphorylation of IκBα and p65 NF‐κB (nuclear factor kappa‐light‐chain‐enhancer of activated B cells), attenuated the expression of Cyclin D1, and cleaved poly(adenosine diphosphate ribose ‐ribose) polymerase in SKOV‐3, A2780, and OVCAR‐3 cells. Furthermore, sanggenol L blocked nuclear translocation of NF‐κB and also attenuated the expression of NF‐κB related genes such as c‐Myc, Cyclin D1, and Bcl‐XL, Bcl‐2, in lipopolysaccharide‐treated SKOV‐3 cells. Overall, our findings for the first time suggest that sanggenol L induces apoptosis via caspase activation and inhibition of NF‐κB/IκBα phosphorylation as a potent chemotherapeutic agent for ovarian cancers. Copyright © 2015 John Wiley & Sons, Ltd. |
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Keywords: | sanggenol L ovarian cancer cells apoptosis PARP caspase 9/3 NF‐κ B |
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