Abstract

Objectives: Interaction of cancer cells with endothelial cells plays an important role in metastasis. Our study hypothesised that SP might play a role in the early onset adhesion of OSCC to HUVEC cells lines via upregulating the adhesion molecule expression.

Methods: CAL 27, SCC25, DOK, H157, BICR22 (OSCC) and HUVEC cell lines were used. Adhesion molecules’ expression was measured by flowcytometry. The ECM645 adhesion assay was used for quantification of tumour-endothelial adhesion. Matrix metalloprotienease-2 (MMP-2) expression in OSCC cells was measured by total ELISA kit.

Results: Treatment with SP increased the adhesion of H157, CAL27 and DOK cells in a time-dependent manner, which was inhibited SP receptor antagonist. Monoclonal anti-adhesion antibodies inhibited the adhesion between OSCC and HUVEC. SP treatment increased (very late antigen-4) VLA-4 adhesion molecule in CAL27 and SCC25 cells and (lymphocyte function associated antigen-1) LFA-1 in BICR22. SP treatment increased MMP-2 release but it was not significant.

Conclusion: The study showed that SP could promote early onset oral cancer–endothelial cell adhesion. The study provided insights into the regulatory mechanism of this adhesion that it can occur in acute phase and in pre-cancer cells. These findings may provide potential new therapeutic targets for metastasis prevention.

Keywords: Oral Squamous Cell Carcinoma; Oral Cancer; Substance P; Tumour-endothelial Adhesion; Adhesion Molecules; NK-1R Antagonist

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Citation

Citation: Moustafa Elhousiny.,et al. “Substance P (SP) Increases the Adhesion of Oral Squamous Cell Carcinoma (OSCC) To Human Umbilical Vein Endothelial Cells (HUVEC) Through Upregulating Adhesion Molecules; Implication for Metastasis”. Acta Scientific Dental Sciences 5.2 (2021): 08-18.

Copyright

Copyright: © 2021 Moustafa Elhousiny.,et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.