Proteomic analysis of changes in the protein composition of MCF-7 human breast cancer cells induced by all-trans retinoic acid, 9-cis retinoic acid, and their combination

被引:14
|
作者
Flodrova, D. [1 ]
Benkovska, D. [1 ]
Macejova, D. [2 ]
Bialesova, L. [2 ]
Hunakova, L. [3 ]
Brtko, J. [2 ]
Bobalova, J. [1 ]
机构
[1] Acad Sci Czech Republ, Inst Analyt Chem, Vvi, Brno 60200, Czech Republic
[2] Slovak Acad Sci, Inst Expt Endocrinol, Bratislava, Slovakia
[3] Slovak Acad Sci, Inst Expt Oncol, Bratislava, Slovakia
关键词
Breast cancer; MCF-7; Biomarker; Retinoids; Proteomics; RECEPTORS; CHEMOPREVENTION; EXPRESSION; REXINOIDS; APOPTOSIS;
D O I
10.1016/j.toxlet.2014.09.030
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Retinoic acid (all-trans and 9-cis) isomers represent important therapeutic agents for many types of cancers, including human breast cancer. Changes in protein composition of the MCF-7 human breast cancer cells were induced by all-trans retinoic acid, 9-cis retinoic acid, and their combination and subsequently proteomic strategies based on bottom-up method were applied. Proposed approach was used for the analysis of proteins extracted from MCF-7 human breast cancer cell line utilizing a commercially manufactured kit RIPA and separated on two dimensional (2D) sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) after treatment with both retinoic acid isomers. We found significant differences in occurrence of proteins probably affecting the cell migration process in tumour cells. Heat shock protein 27, ribonucleoprotein SmD3, and cofilin-1 were significantly upregulated after treatment with combination of individual retinoic acid isomers. On the other hand, AP-5 complex subunit beta-1 shows the different response. Thus, the results might help to find the answer to important medical questions on (i) the identification of signaling pathways affected by retinoic acid isomers or (ii) how the observed proteomic pattern might reflect the effectiveness of retinoic acids treatment. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:226 / 232
页数:7
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