Incorporation of branched-chain fatty acid into cellular lipids and caspase-independent apoptosis in human breast cancer cell line, SKBR-3

Lipids in Health and Disease

Teruyoshi Yanagita³  Takayoshi Toda⁴  Masashi Inafuku¹  Hironori Iwasaki²  Hirosuke Oku²  Sawitree Wongtangtintharn¹ 

[1] United Graduate School of Agricultural Sciences, Kagoshima University, 1-21-24, Korimoto, Kagoshima 890-0065, Japan;Center of Molecular Bioscience, University of the Ryukyus, Nishihara, Okinawa 903-0213, Japan;Department of Applied Biological Sciences, Saga University, Saga 840-8502, Japan;Department of Clinical Laboratory Medicine, University of the Ryukyus Hospital, School of Medicine, Uehara 207, Nishihara, Okinawa 903-0125, Japan

关键词: caspase-independent;    apoptosis;    glycerolipid;    incorporation;    branched-chain fatty acid;   

Others  :  1213236
DOI  :  10.1186/1476-511X-4-29

 received in 2005-10-27, accepted in 2005-11-23,  发布年份 2005

【 摘 要 】

Background

13-Methyltetradecanoic acid (13-MTD), an iso-C15 branched- chain saturated fatty acid, has been shown to induce apoptotic cell death of numerous human cancer cells. However, the mechanism for the induction of apoptosis has not been fully understood. This study described the incorporation of 13-MTD into cellular lipid of SKBR-3 breast cancer cells and apoptosis related event to gain more insight into the mechanism action of this fatty acid.

Results

Treatment of SKBR-3 cells with 13-MTD lowered the cell viability and induced apoptosis. Proportion of 13-MTD in the glycerolipids increased to saturation level within 6 hours. Triacylglycerol contained 13-MTD in higher concentration than phospholipid with positional preference to sn-2. 13-MTD caused no changes in the caspase activity and its gene expression. Furthermore, addition of caspase-inhibitor to culture medium did not prevent the cells from the cytotoxicity of 13-MTD. No-increase in the cellular calcium level was also noted with 13-MTD treatment. However, 13-MTD disrupted the mitochondrial integrity in 4 hours, and increased the nuclear translocation of apoptosis inducing factor.

Conclusion

These results showed that 13-MTD disrupted the mitochondrial integrity, and induced apoptosis via caspase-independent death pathway.

【 授权许可】

   
2005 Wongtangtintharn et al; licensee BioMed Central Ltd.

【 图 表 】

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