Human umbilical cord perivascular cells exhibited enhanced migration capacity towards hepatocellular carcinoma in comparison with bone marrow mesenchymal stromal cells: a role for autocrine motility factor receptor

BAYO FINA, J; MALVICINI, M; FIORE, E; AQUINO, JB; RIZZO, MANGLIO M.; PICCIONI, F; ALANIZ, L; BOLONTRADE, M.F.; PODHAJCER, O. ; GARCÍA, M.G.; MAZZOLINI, G.

Biomed Res int

HINDAWI PUBLISHING CORPORATION

Lugar: New York; Año: 2014

2314-6133

Hepatocellular carcinoma (HCC) is the third cause of cancer-related death in the world. Unfortunately, the incidence and mortality associated with HCC are steadily increasing. Therefore, new therapeutic strategies are urgently needed and the use of mesenchymal stromal cells (MSCs) as carrier of therapeutic genes is emerging as a promising option. Different sources of MSCs are being studied for cell therapy and bone marrow-derived cells are the most extensively explored; however, in the last years, birth associated-tissues represent a very promising source. The aim of this work was to compare the in vitro and in vivo migration capacity between BM-MSCs and human umbilical cord perivascular cells (HUCPVCs) towards HCC and to analyze the mechanisms involved. As a result, we observed that HUCPVCs presented higher in vitro and in vivo migration towards factors released by HCC. We next explored the expression of chemokine´s receptors and observed that autocrine motility factor receptor (AMFR) was increased in HUCPVCs. In addition, genes related with the availability of the receptor on the cell surface (caveolin-1 and -2) and metalloproteinase 3, which is induced by the receptor activation and important for cell migration, were also overexpressed in HUCPVCs. The chemotactic response towards recombinant autocrine motility factor (AMF) was increased in HUCPVCs compared to BM-MSCs, and its inhibition in the CM from HCC induced higher decrease in HUCPVC migration than in BM-MSC. Our results indicate that HUCPVCs could be a useful cellular source to deliver therapeutic genes to HCC.