The role of angiotensin II in cardiovascular disease-induced cancer growth.

Figures

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  Fig. 1. High dose ANGII (2000 ng.kg-1.min-1) induces cardiac hypertrophy and fibrosis (Sham N = 10, ANGII N = 10). A Normalized heart weight. B Masson’s trichome quantification of total cardiac fibrosis. C Representative images of the Masson’s trichome fibrosis staining for total cardiac fibrosis. D Representative echocardiography images on day 20 of ANGII treatment. Data shows mean ± SEM. A-B Two-tailed T-test. HW/BW; heart weight/body weight

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  Fig. 2. LLC tumor growth with and without overlap of ANGII administration. A Experimental design of the ‘ANGII overlap experiment’ (Sham N = 8, ANGII N = 10). B LLC tumor volume over time, C-D tumor volume and weight post-mortem, respectively. E Experimental design of the ‘without ANGII overlap experiment’ (Sham N = 7, ANGII N = 8). F LLC tumor volume over time. G-H Tumor volume and weight post-mortem. Data shows mean ± SEM. B, H Two-way ANOVA test. C-D, G-H Two-tailed T-test

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  Fig. 3. Polyp development in APCmin mice treated with a high dose of ANGII (Sham N = 7, ANGII high dose N = 10). A Polyp count, B normalized heart weight, C cardiac fibrosis, D representative image of polyp growth in the small intestine for the distinct experimental conditions. Arrows indicate more distinctly formed polyps. Data represent mean + SEM. A-C Two-tailed T-test. HW/BW; heart weight to body weight

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  Fig. 4. Polyp development in APCmin mice treated with a low dose of ANGII (Sham N = 7, ANGII low dose N = 7). A Polyp count, B normalized heart weight, C cardiac fibrosis. Data represent mean ± SEM. A-C Two-tailed T-test. HW/BW; heart weight to body weight

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  Fig. 5. MC38 tumor growth when concomitantly treated with ANGII (Sham N = 9, ANGII N = 9). A Differences in AT1 and AT2 mRNA expression in LLC and MC38 tumor cells quantified by qPCR. All expression values are shown relative to LLC AT1 expression. AT1 expression in MC38 tumor cells was significantly lower compared to LLC tumor cells. B Tumor growth over time. C-D tumor volume and weight post-mortem, respectively. Data represents mean ± SEM. A Mann-Whitney test, B Two-way ANOVA, C-D Two-tailed T-test

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  Fig. 6. Percentage of CNV in patient tumors and human cancer cell lines. A Percentage of AT1 CNV in patient tumors as determined by the TCGA database. B Percentage of AT1 CNV in human cancer cell lines. Copy number gain or loss was set as a minimal of one copy number gain or loss. Numbers in parentheses indicate the number of cell lines per cancer type. C LLC cell number when treated with ANGII (10 µg/mL) and/or losartan (0.1 mg/mL) in vitro (N = 2). D Candesartan sensitivity of human cancer cell lines in the Depmap database. Numbers in parentheses indicate the number of cell lines per cancer type. C-D Data show Mean ± SEM. C Kruskal Wallis test. LUSC; Lung squamous cell carcinoma, SCC; squamous cell carcinoma, LUAD; Lung adenocarcinoma, PCPG; Pheochromocytoma and Paraganglioma, CNS; Central nervous system, PNP; Peripheral nervous system