Chelidonium majus L. extract induces apoptosis through caspase activity via MAPK-independent NF-κB signaling in human epidermoid carcinoma A431 cells

Park,Seung-Won; Kim,Seong Ryul; Kim,Youngchul; Lee,Jang-Hoon; Woo,Hong-Jung; Yoon,Yeo-Kwang; Kim,Young Il

doi:10.3892/or.2014.3566

Chelidonium majus L. extract induces apoptosis through caspase activity via MAPK-independent NF-κB signaling in human epidermoid carcinoma A431 cells

Authors:
- Seung-Won Park
- Seong Ryul Kim
- Youngchul Kim
- Jang-Hoon Lee
- Hong-Jung Woo
- Yeo-Kwang Yoon
- Young Il Kim
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Affiliations: Department of Biotechnology, Catholic University of Daegu, Daegu 712-702, Republic of Korea, Department of Agricultural Biology, National Academy of Agricultural Science, Rural Development Administration, Suwon 441-701, Republic of Korea, Department of Internal Medicine, College of Korean Medicine, Kyung Hee University, Seoul 130-872, Republic of Korea, Medical Science Research Institute, Kyung Hee University Medical Center, Seoul 130-872, Republic of Korea
Published online on: October 23, 2014 https://doi.org/10.3892/or.2014.3566
Pages: 419-424

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Abstract

Chelidonium majus L. (C. majus L.) is known to possess certain biological properties such as anti-inflammatory, antimicrobial, antiviral and antitumor activities. We investigated the effects of C. majus L. extract on human epidermoid carcinoma A431 cells through multiple mechanisms, including induction of cell cycle arrest, activation of the caspase-dependent pathway, blocking of nuclear factor-κB (NF-κB) activation and involvement in the mitogen-activated protein kinase (MAPK) pathway. C. majus L. inhibited the proliferation of A431 cells in a dose- and time-dependent manner, increased the percentage of apoptotic cells, significantly decreased the mRNA levels of cyclin D1, Bcl-2, Mcl-1 and survivin and increased p21 and Bax expression. Exposure of A431 cells to C. majus L. extract enhanced the activities of caspase-3 and caspase-9, while co-treatment with C. majus L., the pan-caspase inhibitor Z-VAD-FMK and the caspase-3 inhibitor Z-DEVE-FMK increased the proliferation of A431 cells. C. majus L. extract not only inhibited NF-κB activation, but it also activated p38 MAPK and MEK/ERK signaling. Taken together, these results demonstrate that C. majus L. extract inhibits the proliferation of human epidermoid carcinoma A431 cells by inducing apoptosis through caspase activation and NF-κB inhibition via MAPK-independent pathway.

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