Description
The capacity of melanoma cells to dynamically switch between proliferative and invasive phenotypes is thought to underlie tumor progression, metastasis formation and therapy resistance in melanoma. In this study we identify the low affinity neurotrophin receptor CD271 to play a dual role as a mediator of phenotype switching, more precisely suppressing melanoma cell proliferation while concomitantly promoting metastasis formation in vivo. We therefore did a transcriptome analysis of genes dynamically controlled by CD271 in an experimental set-up mimicking reversible phenotype switching. We sequenced RNA of human melanoma cells before, during and after induced CD271 overexpression to find a transiently expressed gene set regulated by CD271 that could explain the phenotype switch observed upon temporal CD271 overexpression.