Fig 2: Immunohistochemical staining for the AT1R (A), AT2R (B), and MasR (C) in control and captopril treated animals at day 16 and day 21. AT1R localised to cells within the stromal intrusions of CRC metastases with light staining also observed in tumor cells at the periphery (A). There appeared to be a greater number of AT1R-positive cells in and around CRC metastases in control compared to the captopril treated animals, supporting mRNA analysis for this receptor (Figure 2). AT2R protein localized to tumor cells only with no staining evident in the liver (B). MasR staining was found within and around the necrotic centre of CRC metastases and a greater number of MasR staining was observed in control groups as compared to the captopril treated groups (similar to the mRNA data presented in Figure 2). As with the AT2R, MasR staining was only evident in tumor cells.

Fig 3: The mitochondrial assembly receptor (MasR) antagonist reversed the inhibition of tongue cancer cell growth induced by angiotensin-(1-7). (a) and (b) Serum-starved HSC-3 and Cal27 cells were pretreated with or without A779 for 24 h following stimulation with angiotensin-(1-7). The cells were then cultured for 72 h and then subjected to 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and bromodeoxyuridine (BrdU) incorporation assays to quantitate cell growth.*p<0.05; **p<0.01; ***p<0.001.

Fig 4: Immunohistochemical staining of mitochondrial assembly receptors (MasRs): (a) low expression of MasR; (b) overexpression of MasR. Original magnification ×200.