Involvement of TIMP-1 in PECAM-1-mediated tumor dissemination

International Journal of Oncology
Valsamma AbrahamHorace M DeLisser

Abstract

Platelet endothelial cell adhesion molecule‑1 (PECAM‑1) is expressed on the vascular endothelium and has been implicated in the late progression of metastatic tumors. The activity of PECAM‑1 appears to be mediated by modulation of the tumor microenvironment (TME) and promotion of tumor cell proliferation, rather than through the stimulation of tumor angiogenesis. The present study aimed to extend those initial findings by indicating that the presence of functional PECAM‑1 on the endothelium promotes a proliferative tumor cell phenotype in vivo, as well as in tumor cell (B16‑F10 melanoma and 4T1 breast cancer cell lines) co‑culture assays with mouse endothelial cells (ECs) or a surrogate EC line (REN‑MP). The pro‑proliferative effects were mediated by soluble endothelial‑derived factors that were dependent on PECAM‑1 homophilic ligand interactions, but which were independent of PECAM‑1‑dependent signaling. Further analysis of the conditioned media obtained from tumor/EC and tumor/REN‑MP co‑cultures identified TIMP metallopeptidase inhibitor‑1 (TIMP‑1) as a PECAM‑1‑regulated factor, the targeting of which in the tumor cell/REN‑MP system inhibited tumor cell proliferation. In addition, TIMP‑1 expression was decreased in metastatic...Continue Reading

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Citations

Jul 4, 2020·Genesis : the Journal of Genetics and Development·Donghua HuChen-Leng Cai
Apr 10, 2019·Marine Drugs·Huai-Ching TaiShih-Wei Wang

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Methods Mentioned

BETA
glycosylation
fluorescent-activated cell sorting
flow cytometry
antibody
FACS
ELISA
protein assay

Software Mentioned

GraphPad
ImageJ
GraphPad Prism
Excel
FlowJo

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