Induction of apoptosis by deinoxanthin in human cancer cells.

Abstract

BACKGROUND:

Deinoxanthin is unique carotenoid isolated from the radioresistant bacterium Deinococcus radiodurans. In the present study, the induction of apoptosis of cancer cells by deinoxanthin was investigated.

MATERIALS AND METHODS:

Apoptotic effects were evaluated in HepG2, PC-3, and HT-29 cells, and were measured through cell viability, morphological changes, and a DNA fragmentation assay. Intracellular generation of reactive oxygen species (ROS) was measured using 5-(and 6-)-carboxy-2',7'-dichlorodihydrofluorescein diacetate (carboxy-H2DCF-DA). The expression of apoptotic and anti-apoptotic proteins was assayed by western blotting.

RESULTS:

The half-maximal inhibitory concentration (IC50) values for deinoxanthin against the HepG2, HT-29, and PC-3 cell lines were 59 μM, 61 μM, and 77 μM, respectively. Deinoxanthin treatment caused an increase in ROS in all tested cells, suggesting possible pro-oxidant activity of deinoxanthin. Pro-caspase-3 was degraded in cancer cells by deinoxanthin treatment. Moreover, BCL2 expression decreased, but that of BAX increased.

CONCLUSION:

The present findings demonstrate for the first time the novel functional property of deinoxanthin isolated from radioresistant bacteria as a potent inducer of apoptosis in cancer cells. These data suggest that deinoxanthin could be potentially useful as a chemopreventive agent.

• Authors: Yong-Ji Choi, Jung-Mu Hur, Sangyong Lim, Minho Jo, Dong Ho Kim, Jong-Il Choi
• Journal: Anticancer research (Anticancer Res) Vol. 34 Issue 4 Pg. 1829-35 (Apr 2014) ISSN: 1791-7530 [Electronic] Greece
• PMID: 24692716 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antineoplastic Agents
• Proto-Oncogene Proteins c-bcl-2
• Reactive Oxygen Species
• deinoxanthin
• Carotenoids
• Caspase 3

Topics

• Antineoplastic Agents (pharmacology)
• Apoptosis (drug effects)
• Carotenoids (pharmacology)
• Caspase 3 (metabolism)
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Cell Survival (drug effects)
• Enzyme Activation (drug effects)
• Humans
• Proto-Oncogene Proteins c-bcl-2 (metabolism)
• Reactive Oxygen Species (metabolism)