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Volume 92, Issue 3, Pages 353-361 (September 2009)


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CD133 expression is not selective for tumor-initiating or radioresistant cell populations in the CRC cell lines HCT-116

Claudia Dittfelda1, Antje Dietricha1, Susann Peickerta, Sandra Heringb, Michael Baumanncd, Marian Gradee, Thomas Riedf, Leoni A. Kunz-SchughartaCorresponding Author Informationemail address

Received 28 April 2009; received in revised form 17 June 2009; accepted 24 June 2009. published online 25 August 2009.

Abstract 

Background and purpose

CD133 is controversially discussed as putative (surrogate) marker for cancer stem/tumor-initiating cell populations (CSC/TIC) in epithelial tumors including colorectal carcinomas (CRCs). We studied CD133 expression in established CRC cell lines and examined in vitro behavior, radioresponse and in vivo tumor formation of CD133+/− subpopulations of one cell line of interest.

Materials and methods

Ten CRC cell lines were analyzed for CD133 expression using flow cytometry and Western blotting. CD133+ and CD133 HCT-116 subpopulations were separated by FACS and studied in 2-D and 3-D culture and colony formation assays after irradiation. Subcutaneous xenograft formation was monitored in NMRI (nu/nu) mice.

Results and conclusions

CRC cell lines could be classified into three groups: (i) CD133, (ii) CD133+ and (iii) those with two distinct CD133+ and CD133 subpopulations. Isolated CD133+/− HCT-116 subpopulations were studied relative to the original fraction. No difference was found in 2-D growth, spheroid formation or radioresponse in vitro. Also, tumor formation and growth rate did not differ for the sorted subpopulations. However, a subset of xenografts originated from CD133 HCT-116 showed a striking enrichment in the CD133+ fraction. Our data show that CD133 expression is not selective for sphere forming, tumor-initiating or radioresistant subpopulations in the HCT-116 CRC cell lines. This implies that CD133 cannot be regarded as a CSC/TIC marker in all CRC cell lines and that functional measurements of tumor formation have to generally accompany CSC/TIC-directed mechanistic or therapeutic studies.

a Tumor Pathophysiology, OncoRay – Center for Radiation Research in Oncology, Dresden University of Technology, Germany

b Institute of Legal Medicine, Dresden University of Technology, Germany

c OncoRay – Center for Radiation Research in Oncology, Dresden University of Technology, Germany

d Department of Radiation Oncology, University Hospital Dresden, Germany

e Department of General and Visceral Surgery, University Medicine Goettingen, Germany

f National Cancer Institute, National Institutes of Health, Bethesda, MD, USA

Corresponding Author InformationCorresponding author. Address: OncoRay – Center for Radiation Research in Oncology, Faculty of Medicine Carl Gustav Carus, Dresden University of Technology, Fetscherstraße 74, PF 86, 01307 Dresden, Germany.

1 Contributed equally.

PII: S0167-8140(09)00338-7

doi:10.1016/j.radonc.2009.06.034


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