Oncotarget

Research Papers:

CD271 is an imperfect marker for melanoma initiating cells

Yann Cheli, Vanessa F. Bonnazi, Arnaud Jacquel, Maryline Allegra, Gian Marco De Donatis, Philippe Bahadoran, Corine Bertolotto and Robert Ballotti _

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Oncotarget. 2014; 5:5272-5283. https://doi.org/10.18632/oncotarget.1967

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Abstract

Yann Cheli1,2, Vanessa F. Bonnazi1,2, Arnaud Jacquel4,2, Maryline Allegra1,2,3, Gian Marco De Donatis1,2, Philippe Bahadoran1,2,3,5, Corine Bertolotto1,2,3 and Robert Ballotti1,2,3

1 INSERM U1065, Equipe 1, Biologie et pathologies des mélanocytes: de la pigmentation cutanée au mélanome, Equipe labellisée Ligue 2013, Centre Méditerranéen de Médecine Moléculaire, Nice, France

2 Université de Nice Sophia-Antipolis, UFR Médecine, Nice, France

3 CHU Nice, Service de Dermatologie, Nice, France

4 INSERM U1065, Equipe 2, Cell death, differentiation and cancer, Centre Méditerranéen de Médecine Moléculaire, Nice, France

5 CHU Nice, Clinical Research Center, Nice, France

Correspondence:

Robert Ballotti, email:

Keywords: Melanoma initiating cells, CD271, slow growing, MITF

Received: March 20, 2014 Accepted: May 12, 2014 Published: May 13, 2014

Abstract

Understanding the molecular and cellular processes underlying melanoma plasticity and heterogeneity is of paramount importance to improve the efficiency of current treatment and to overcome resistance to chemotherapy drugs. The notion of plasticity and heterogeneity implies the existence of melanoma cell populations with different phenotypic and tumorigenic properties.

Using melanoma cell lines and melanoma cells freshly isolated from patient biopsies, we investigated the relationship between ABCB5+, CD271+ and low-MITF, expressing populations that were reported to display melanoma initiating cell properties. Here, we showed that ABCB5+ and CD271+ populations poorly overlap. However, we found that the CD271+ population is enriched in low-MITF cells and expresses a higher level of stemness genes, such as OCT4, NANOG and NES. These features could explain the increased tumorigenicity of the CD271+ cells. The rapid conversion of CD271+ to CD271- cells in vitro demonstrates the plasticity ability of melanoma cells. Finally, we observed that the transient slow-growing population contains only CD271+ cells that are highly tumorigenic. However, the fast growing/CD271+ population exhibits a poor tumorigenic ability. Taking together, our data show that CD271 is an imperfect marker for melanoma initiating cells, but may be useful to identify melanoma cells with an increased stemness and tumorigenic potential.


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