Cardiovascular disease (CVD) and cancer are two major causes of death worldwide. The question is, “Could there be a link between these two pathologies in addition to their shared, common risk factors?” To find some answers, we studied the effect of oxidized low-density lipoproteins (oxLDL) on head and neck cancer (HNC) cell lines, since oxLDL is a major contributor to atherosclerosis and the principal cause of CVD. In this study, we exposed three HNC cell lines (Detroit 562, UPCI-SCC-131 and FaDu) to oxLDL. We investigated two oxLDL receptors, CD36 and Lox-1, using immunofluorescence. Cancer cell migration was evaluated using Boyden chambers and the Wnt/β-catenin pathway was investigated using Western blotting. We demonstrated that the expression of CD36 and Lox-1 significantly increases after exposure to oxLDL. Moreover, we found that oxLDL reduces the migration of HNC cell lines, an observation that is in line with an increased degradation of β-catenin under oxLDL. Finally, the inhibition of CD36 with sulfosuccinimidyl oleate (SSO) reverses the inhibition of cell migration. In conclusion, we report that oxLDL seems to induce an increase in CD36 expression on HNC cell lines, enhancing the uptake of these lipids in cells to finally decrease cancer cell migration via the CD36/β-catenin pathway.

Cardiovascular diseases (CVD) and cancers are the two main causes of death worldwide. The initiation and progression of atherosclerosis is, in large part, caused by oxidized low-density lipoproteins (oxLDL); interestingly, oxLDL may also play a role in cancer cell metabolism and migration. As oxLDL are generally obtained by tedious ultracentrifugation procedures, “home-made” oxLDL were obtained by (i) applying a purification kit to isolate LDL and VLDL from human plasma; (ii) isolating LDL from VLDL by gel permeation chromatography (GPC); and (iii) oxidating LDL through CuSO4 incubation. On three HPV-positive head and neck cancer cells (HNCC) (93VU-147T, UM-SCC47, and UPCI-SCC154), cell migration was assessed using Boyden chambers, the Wnt/ß-catenin pathway was analyzed by Western Blotting, and the expression of two oxLDL receptors, LOX-1 and CD36, in response to oxLDL exposure, was analysed by immunofluorescence. Our data indicate: (a) a non-significant difference between reference and “home-made” oxLDL; (b) a decreased migration, parallel to an inhibition of the ß-catenin pathway; and (c) an increase of CD36 and LOX-1 expression in all HNCC. In conclusion, we successfully produced oxLDL. Our results demonstrate a decrease in HNCC migration after oxLDL exposure, and an increased expression of LOX-1 and CD36 associated with lipid uptake.

Central blood pressure (cBP) is known to be a better predictor of the damage caused by hypertension in comparison with peripheral blood pressure. During cardiac catheterization, we measured cBP in the ascending aorta with a fluid-filled guiding catheter (FF) in 75 patients and with a high-fidelity micromanometer tipped wire (FFR) in 20 patients. The wire was withdrawn into the brachial artery and aorto-brachial pulse wave velocity (abPWV) was calculated from the length of the pullback and the time delay between the ascending aorta and the brachial artery pulse waves by gating to the R-wave of the ECG for both measurements. In 23 patients, a cuff was inflated around the calf and an aorta-tibial pulse wave velocity (atPWV) was calculated from the distance between the cuff around the leg and the axillary notch and the time delay between the ascending aorta and the tibial pulse waves. Brachial BP was measured non-invasively and cBP was estimated using a new suprasystolic oscillometric technology. The mean differences between invasively measured cBP by FFR and non-invasive estimation were −0.4 ± 5.7 mmHg and by FF 5.4 ± 9.4 mmHg in 52 patients. Diastolic and mean cBP were both overestimated by oscillometry, with mean differences of −8.9 ± 5.5 mmHg and −6.4 ± 5.1 mmHg compared with the FFR and −10.6 ± 6.3 mmHg and −5.9 ± 6.2 mmHg with the FF. Non-invasive systolic cBP compared accurately with the high-fidelity FFR measurements, demonstrating a low bias (≤5 mmHg) and high precision (SD ≤ 8 mmHg). These criteria were not met when using the FF measurements. Invasively derived average Ao-brachial abPWV was 7.0 ± 1.4 m/s and that of Ao-tibial atPWV was 9.1 ± 1.8 m/s. Non-invasively estimated PWV based on the reflected wave transit time did not correlate with abPWV or with atPWV. In conclusion, we demonstrate the advantages of a novel method of validation for non-invasive cBP monitoring devices using acknowledged gold standard FFR wire transducers and the possibility to easily measure PWV during coronary angiography with the impact of cardiovascular risk factors.

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