Exogenous coenzyme Q10 modulates MMP-2 activity in MCF-7 cell line as a breast cancer cellular model

Nutrition Journal

Research

Shahnaz Khaghani¹  Massih Bahar¹  Siavash Gerayesh Nejad¹  Parvin Pasalar¹  Maliheh Paknejad¹  Mohammad Reza Khorramizadeh²  Hossein Mirmiranpour² 

[1] Department of Clinical Biochemistry, Tehran University of Medical Sciences, Faculty of Medicine, Tehran, Iran;Department of Pathology, Tehran University of Medical Sciences, Faculty of Public Health, Tehran, Iran;

关键词: H2O2 Content;    Buthionine Sulfoximine;    Monothiol;    Thiol Antioxidant;    Cysteine Switch;   

DOI  :  10.1186/1475-2891-9-62

 received in 2010-05-29, accepted in 2010-11-30,  发布年份 2010

来源: Springer

【 摘 要 】

Background/AimsMatrix Metalloproteinases 2 is a key molecule in cellular invasion and metastasis. Mitochondrial ROS has been established as a mediator of MMP activity. Coenzyme Q10 contributes to intracellular ROS regulation. Coenzyme Q10 beneficial effects on cancer are still in controversy but there are indications of Coenzyme Q10 complementing effect on tamoxifen receiving breast cancer patients.MethodsIn this study we aimed to investigate the correlation of the effects of co-incubation of coenzyme Q10 and N-acetyl-L-cysteine (NAC) on intracellular H2O2 content and Matrix Metalloproteinase 2 (MMP-2) activity in MCF-7 cell line.Results and DiscussionOur experiment was designed to assess the effect in a time and dose related manner. Gelatin zymography and Flowcytometric measurement of H2O2 by 2'7',-dichlorofluorescin-diacetate probe were employed. The results showed that both coenzyme Q10 and N-acetyl-L-cysteine reduce MMP-2 activity along with the pro-oxidant capacity of the MCF-7 cell in a dose proportionate manner.ConclusionsCollectively, the present study highlights the significance of Coenzyme Q10 effect on the cell invasion/metastasis effecter molecules.

【 授权许可】

Unknown   
© Bahar et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.