The Interplay between Atherosclerosis and Cancer: Breast Cancer Cells Increase the Expression of Endothelial Cell Adhesion Markers

• Published in: Biology (Basel, Switzerland) Vol. 12; no. 7; p. 896
• Main Authors: Scalia, Alessandro, Doumani, Lesly, Kindt, Nadège, Journé, Fabrice, Trelcat, Anne, Carlier, Stéphane
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 22.06.2023; MDPI
• Subjects: Arteries; Arteriosclerosis; Atherosclerosis; Blood lipids; Breast cancer; Cancer; Cancer cells; Cardiovascular diseases; CD36 antigen; Cell adhesion; Cell adhesion & migration; Cell growth; Cholesterol; Chromatography; conditioned medium; Connexin 43; E-selectin; Endothelial cells; Endothelium; Growth factors; Hypoxia; Immunofluorescence; Intercellular adhesion molecule 1; Leukemia; Lipoproteins; Low density lipoprotein; Low density lipoproteins; LOX-1 protein; Lung cancer; Monocytes; Oncology, Experimental; Oxidation; oxLDL; Penicillin; Phosphatase; Photographic industry; THP-1; Tumor cell lines; Umbilical vein; Veins & arteries; Belgium; Massachusetts; Japan; United Kingdom > UK; United States > US; atherosclerosis; conditioned medium; oxLDL; oxidation; THP-1; breast cancer
• ISSN: 2079-7737; 2079-7737
• DOI: 10.3390/biology12070896

Cardiovascular diseases are the leading causes of death worldwide, closely followed by cancer. To investigate the impact of breast cancer cell lines (SKBR3, MCF-7, and MDA-MB-231) on endothelial cell adhesion, a blended medium containing 30% breast-cancer-conditioned medium was prepared. This medium was then exposed to human umbilical vein endothelial cells (HUVECs) and monocytes (THP-1) for 48 h. Homemade oxidized low-density lipoproteins (oxLDL) were optionally added to the blended medium. Immunofluorescence was performed to assess the expression of E-selectin, connexin-43, and ICAM-1 on HUVECs, as well as LOX-1, CD36, and CD162 on THP-1. Additionally, unoxidized LDL was exposed to the three breast cancer cell lines for 48 h, and the formation of oxLDL was quantified. Our results revealed an upregulation of all six adhesion markers involved in the initiation of atherosclerosis when HUVECs and THP-1 were exposed to the breast-cancer-conditioned medium. Furthermore, this expression was further increased by exposure to oxLDL. We also observed a significant elevation in oxLDL levels when LDL was exposed to breast cancer cells. In conclusion, our findings successfully demonstrate an increased LDL oxidation in the presence of breast cancer cells, accompanied by an augmented expression of receptors involved in atherosclerosis initiation. These findings shed new light on the clinically observed interplay between atherosclerosis and cancer.