The convergent roles of CD271/p75 in neural crest-derived melanoma plasticity

Abstract

The embryonic microenvironment is an important source of signals that promote multipotent cells to adopt a specific fate and direct cells along distinct migratory pathways. Yet, the ability of the embryonic microenvironment to retain multipotent progenitors or reprogram de-differentiated cells is less clear. Mistakes in cell differentiation or migration often result in developmental defects and tumorigenesis, including aggressive cancers that share many characteristics with embryonic progenitor cells. This is a striking feature of the vertebrate neural crest, a multipotent and highly migratory cell population first identified by His (1868) with the potential to metamorphose into aggressive melanoma cancer. In this perspective, we address the roles of CD271/p75 in tumor initiation, phenotype switching and reprogramming of metastatic melanoma and discuss the convergence of these roles in melanoma plasticity.

Keywords: CD271; Melanoma; Microenvironment; NGF; Neural crest; p75.

Figure 1

Convergence of the roles of CD271/p75 in melanoma plasticity. (A, Phenotype switching) CD271 as a regulator of phenotype switching in melanoma. (B, Tumor initiating cell marker) CD271 as a marker for tumor initiating cells. (C, Reprogramming potential) NGF-induced MART1 as a marker of melanoma reprogramming of CD271-positive cells to a less aggressive cell type.