Recent evidence has shown that Angiotensin II (Ang II) can stimulate growth in a number of different cell lines. We looked at the expression of MMP‐2, annexin V, and the Ang II receptor, AT1, to determine if these proteins are differentially regulated in normal (MC3T3) and cancerous (K7MZ) mouse bone cells. MMP‐2 has been shown to increase inflammation and metastasis, whereas annexin V has been linked to apoptosis. In order to assess whether the differences in MMP‐2 and annexin V expression were mediated by AT1, and to confirm that the Ang II produced in these cells acts via an intracrine pathway, we measured AT1 by Western blot analysis. In MC3T3 cells there was little change in MMP‐2 expression between control and the Ang II expressing cells. K7MZ mouse osteoblasts showed an increase in MMP‐2 expression as compared to the MC3T3 cells as well as an increase in expression between control and experimental (Ang II expressing) within the cell line. Cancer cells down regulate genes responsible for inducing apoptosis. Our data are consistent with this model as the K7MZ cells showed a marked decrease in annexin V expression in cells expressing angiotensin II directly. AT1 expression was not affected in either cell line by direct expression of Ang II. These data suggest that Ang II may play a role in the growth of cancer cells, and their ability to metastasize and avoid apoptosis.