
CD15 Expression Does Not Identify a Phenotypically or Genetically Distinct Glioblastoma Population
Author(s) -
Kenney-Herbert Emma,
Al-Mayhani Talal,
Piccirillo Sara G.M.,
Fowler Joanna,
Spiteri Inmaculada,
Jones Philip,
Watts Colin
Publication year - 2015
Publication title -
stem cells translational medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.781
H-Index - 71
eISSN - 2157-6580
pISSN - 2157-6564
DOI - 10.5966/sctm.2014-0047
Subject(s) - cd15 , biology , population , cancer stem cell , stem cell , cancer research , microbiology and biotechnology , immunology , genetics , medicine , environmental health , cd34
Recent research has focused on the hypothesis that the growth and regeneration of glioblastoma (GB) is sustained by a subpopulation of self‐renewing stem‐like cells. This has led to the prediction that molecular markers for cancer stem cells in GB may provide a treatment target. One candidate marker is CD15: we wanted to determine if CD15 represented a credible stem cell marker in GB. We first demonstrated that CD15‐positive (CD15+) cells were less proliferative than their CD15‐negative (CD15−) counterparts in 10 patient GB tumors. Next we compared the proliferative activity of CD15+ and CD15− cells in vitro using tumor‐initiating primary GB cell lines (TICs) and found no difference in proliferative behavior. Furthermore, TICs sorted for CD15+ and CD15− were not significantly different cytogenetically or in terms of gene expression profile. Sorted single CD15+ and CD15− cells were equally capable of reconstituting a heterogeneous population containing both CD15+ and CD15− cells over time, and both CD15+ and CD15− cells were able to generate tumors in vivo. No difference was found in the phenotypic or genomic behavior of CD15+ cells compared with CD15− cells from the same patient. Moreover, we found that in vitro, cells were able to interconvert between the CD15+ and CD15− states. Our data challenge the utility of CD15 as a cancer stem cell marker. Significance The data from this study contribute to the ongoing debate about the role of cancer stem cells in gliomagenesis. Results showed that CD15, a marker previously thought to be a cancer stem‐like marker in glioblastoma, could not isolate a phenotypically or genetically distinct population. Moreover, isolated CD15‐positive and ‐negative cells were able to generate mixed populations of glioblastoma cells in vitro.