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ORIGINAL ARTICLE
Year : 2012  |  Volume : 8  |  Issue : 3  |  Page : 399-403

Cell cycle analysis of the CD133 + and CD133 - cells isolated from human colorectal cancer


1 Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
2 Department of Gasteroentrology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
3 Department of Pathology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
4 Department of Biostatistics and Epidemiology, School of Public Health, Isfahan University of Medical Sciences, Isfahan, Iran
5 Department of Surgery, Alzahra University Hospital, Isfahan University of Medical Sciences, Isfahan, Iran

Correspondence Address:
Marjan Gharagozloo
Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan
Iran
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-1482.103520

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Aim: The CD133 antigen has been identified as a putative stem cell marker in colorectal cancer tissues. The aim of this study was to investigate the cell cycle state of CD133 + and CD133 - cells, isolated from primary human colorectal tumors. Materials and Methods: After mechanical and enzymatic dissociation of the tumor samples, CD133 + and CD133 - subsets were identified and separated by magnetic cell sorting. Flow cytometric analysis was performed to compare the cell cycle of both CD133 + and CD133 - cells isolated from primary and liver metastatic cancer cells. Results: The results indicated that CD133 + cells isolated from both primary and liver metastatic colorectal cancers were found in higher percentage in the G0/G1 phases. However, the CD133 - cells isolated from primary colorectal cancers were predominantly found in the S and G2/M phases. Surprisingly, the CD133 - cells isolated from liver metastatic colorectal cancers were mostly found in the G0/G1 phase. Conclusion: The present study provides evidence that CD133 + cells are in a quiescent state in colorectal cancer, representing a mechanism that would at least partially explain chemotherapy resistance and tumor recurrence in post-therapy patients.


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