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ORIGINAL ARTICLE
Year : 2017  |  Volume : 12  |  Issue : 1  |  Page : 67-73

Imatinib and its combination with 2,5-dimethyl-celecoxibinduces apoptosis of human HT-29 colorectal cancer cells


1 Department of Biochemistry, Student Research Committee, Urmia University of Medical Sciences, Urmia, Iran
2 Department of Biochemistry, Urmia University of Medical Sciences, Urmia, Iran
3 Department of Pharmacology, Cellular and Molecular Research Center, Urmia University of Medical Sciences, Urmia, Iran
4 Department of Clinical Biochemistry, Cellular and Molecular and Solid Tumor Research Center, Urmia University of Medical Sciences, Urmia, Iran

Correspondence Address:
Fatemeh Kheradmand
Department of Clinical Biochemistry, Cellular and Molecular and Solid Tumor Research Center, Urmia University of Medical Sciences, Urmia
Iran
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1735-5362.199049

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Mono-targeting by imatinib as a main antitumor agent does not always accomplish complete cancer suppression. 2,5-dimethyl-celecoxib (DMC) is a close structural analog of the selective cyclooxygenase-2 (COX-2) inhibitor, celecoxib, that lacks COX-2 inhibitory function. In this study, we aimed to show the apoptotic effects of imatinib in combination with DMC in human HT-29 colorectal cancer (CRC) cells. HT-29 CRC cells were treated with IC 50 dose of imatinib (6.60 μM), DMC (23.45 μM), and their combination (half dose of IC 50 ) for 24 h. The caspase-3 activity was estimated with colorimetric kit. The caspase-3 gene expression was evaluated by real-time PCR method. There was a significant up-regulation in caspase-3 enzyme activity and caspase-3 expression by imatinib and its half dose combination with DMC as compared to control. As a summary, the results of this study strongly suggest that half dose combination of imatinib with DMC induced apoptosis as potent as full dose imatinib in human HT-29 CRC cells, while minimizing undesired side effects related to imatinib mono-therapy. This study also pointed towards possible caspase-dependent actions of imatinib and DMC.


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