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In Vitro Cell Dev Biol Anim. 2015 Jan;51(1):92-101. doi: 10.1007/s11626-014-9806-6. Epub 2014 Aug 23.

[10]-Gingerol induces mitochondrial apoptosis through activation of MAPK pathway in HCT116 human colon cancer cells.

Author information

1
Department of Foods and Nutrition, College of Natural Sciences, Duksung Women's University, Seoul, 132-714, Republic of Korea.

Abstract

The present study was designed to investigate the molecular mechanisms of [10]-gingerol activity against HCT116 human colon cancer cells. [10]-Gingerol inhibited the proliferation of HCT116 cells by 50% at a concentration of 30 μM, and this inhibition was dose-dependent accompanied by the morphological changes indicative of apoptosis. Furthermore, flow cytometric analysis showed that [10]-gingerol increased DNA in the sub-G1 phase of the cell cycle, and the extent of apoptosis was confirmed by Annexin V and PI double staining. Analysis of the mechanism of these events indicated that [10]-gingerol-treated cells exhibited an increased ratio of Bax/Bcl-2, resulting in the activation of caspase-9, caspase-3, and poly-ADP-ribose polymerase in a dose-dependent manner, which are hallmarks of apoptosis. Moreover, [10]-gingerol-induced apoptosis was accompanied by phosphorylation of the mitogen-activated protein kinase (MAPKs) family, c-Jun N-terminal kinase (JNK), p38 MAPK (p38), and extracellular signal-regulated kinase (ERK). This is the first report to demonstrate the cytotoxic effect of [10]-gingerol on human colon cancer cells, as well as the first to describe its possible chemotherapeutic potentials.

PMID:
25148824
DOI:
10.1007/s11626-014-9806-6
[Indexed for MEDLINE]

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