Abstract：
:Targeting the vasculature remains a promising approach for treating solid tumours; however, the mechanisms of tumour neovascularization are diverse and complex. Here we uncover a new subpopulation of melanoma cells that express the vascular cell adhesion molecule PECAM1, but not VEGFR-2, and participate in a PECAM1-dependent form of vasculogenic mimicry (VM). Clonally derived PECAM1(+) tumour cells coalesce to form PECAM1-dependent networks in vitro and they generate well-perfused, vascular endothelial growth factor (VEGF)-independent channels in mice. The neural crest specifier AP-2α is diminished in PECAM1(+) melanoma cells and is a transcriptional repressor of PECAM1. Re-introduction of AP-2α into PECAM1(+) tumour cells represses PECAM1 and abolishes tube-forming ability, whereas AP-2α knockdown in PECAM1(-) tumour cells upregulates PECAM1 expression and promotes tube formation. Thus, VM-competent subpopulations, rather than all cells within a tumour, may instigate VM, supplant host-derived endothelium, and form PECAM1-dependent conduits that are not diminished by neutralizing VEGF.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Dunleavey JM,Xiao L,Thompson J,Kim MM,Shields JM,Shelton SE,Irvin DM,Brings VE,Ollila DW,Brekken RA,Dayton PA,Melero-Martin JM,Dudley ACdoi
10.1038/ncomms6200subject
Has Abstractpub_date
2014-10-22 00:00:00pages
5200issn
2041-1723pii
ncomms6200journal_volume
5pub_type
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