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Cancers (Basel). 2019 Jul 8;11(7). pii: E956. doi: 10.3390/cancers11070956.

Transient Receptor Potential Channel Expression Signatures in Tumor-Derived Endothelial Cells: Functional Roles in Prostate Cancer Angiogenesis.

Author information

1
Univ. Lille, Inserm, U1003-PHYCEL-Physiologie Cellulaire, F-59000 Lille, France.
2
Laboratory of Excellence, Ion Channels Science and Therapeutics, Université de Lille, F-59655 Villeneuve d'Ascq, France.
3
Department of Life Science and Systems Biology, University of Torino, 10123 Turin, Italy.
4
Department of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Centre, University of Torino, 10126 Turin, Italy.
5
Univ. Lille, Institut Français de Bioinformatique, bilille, F-59000 Lille, France.
6
Univ. Lille, Inria, CHU Lille, EA 2694-MODAL-Models for Data Analysis and Learning, F-59000 Lille, France.
7
Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8161, F-59000 Lille, France.
8
Inserm UMR 1069, Université de Tours, 37000 Tours, France.
9
Univ. Lille, Inserm, U1003-PHYCEL-Physiologie Cellulaire, F-59000 Lille, France. dimitra.gkika@univ-lille.fr.
10
Laboratory of Excellence, Ion Channels Science and Therapeutics, Université de Lille, F-59655 Villeneuve d'Ascq, France. dimitra.gkika@univ-lille.fr.

Abstract

Background: Transient receptor potential (TRP) channels control multiple processes involved in cancer progression by modulating cell proliferation, survival, invasion and intravasation, as well as, endothelial cell (EC) biology and tumor angiogenesis. Nonetheless, a complete TRP expression signature in tumor vessels, including in prostate cancer (PCa), is still lacking. Methods: In the present study, we profiled by qPCR the expression of all TRP channels in human prostate tumor-derived ECs (TECs) in comparison with TECs from breast and renal tumors. We further functionally characterized the role of the 'prostate-associated' channels in proliferation, sprout formation and elongation, directed motility guiding, as well as in vitro and in vivo morphogenesis and angiogenesis. Results: We identified three 'prostate-associated' genes whose expression is upregulated in prostate TECs: TRPV2 as a positive modulator of TEC proliferation, TRPC3 as an endothelial PCa cell attraction factor and TRPA1 as a critical TEC angiogenic factor in vitro and in vivo. Conclusions: We provide here the full TRP signature of PCa vascularization among which three play a profound effect on EC biology. These results contribute to explain the aggressive phenotype previously observed in PTEC and provide new putative therapeutic targets.

KEYWORDS:

TRP; calcium channel; migration; prostate cancer; tumor angiogenesis

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