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Oncol Lett. 2018 Nov;16(5):6039-6044. doi: 10.3892/ol.2018.9379. Epub 2018 Sep 3.

Antitumorigenic effect of damnacanthal on melanoma cell viability through p53 and NF-κB/caspase-3 signaling pathways.

Author information

1
Department of Dermatology, Chinese People's Liberation Army General Hospital, Beijing 100853, P.R. China.
2
Department of Medical Oncology, Chinese People's Liberation Army General Hospital, Beijing 100853, P.R. China.

Abstract

Melanoma is highly malignant, particularly prone to metastasizing to the skin. The incidence of melanoma varies markedly between countries, and is relatively low in China. The aim of the present study was to investigate the antitumorigenic effect of damnacanthal on melanoma cells, and its molecular mechanism. MUM-2B cells were treated with 0-20 µM damnacanthal for 12, 24 and 48 h. In vitro, it was demonstrated that damnacanthal inhibited proliferation and promoted apoptosis of melanoma cells in a dose- and time-dependent manner. Damnacanthal treatment increased caspase-3/8 and 9 activity, and promoted B-cell lymphoma 2-associated X protein, tumor protein p53 (p53) and p21 protein expression levels in melanoma cells. Damnacanthal treatment also resulted in downregulated nuclear factor-κB (NF-κB), cyclin D and cyclin E protein expression in melanoma cells. In conclusion, the results of the present study demonstrated that the antitumorigenic activity of damnacanthal on melanoma cells is executed via the p53/p21 and NF-κB/cyclin/ caspase-3 signaling pathways.

KEYWORDS:

damnacanthal; melanoma; nuclear factor-κB; tumor protein p53

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