It is becoming increasingly clear that a prostate cancer cell's microenvironment is crucial to its survival, progression, and metastasis. However, the mechanisms by which the tumor cell interacts with its surroundings are largely unidentified. Experiments have shown that the growth of prostate carcinoma cells can be either inhibited or stimulated by specific stromal environments. Angiogenesis, a critical factor in cancer progression, is likewise stromally-mediated. As many of the cellular and humoral factors involved in angiogenesis are also significant to the process of wound healing, the “reactive stroma” of a malignant tumor may parallel the granulation tissue of a healing wound in many ways, thereby facilitating the development of valuable experimental models. Metastasis to bone, perhaps the most clinically significant aspect of prostate cancer, is also dependent on stromal–epithelial crosstalk, as prostate carcinoma cells must induce the hospitality of bone cells in order to take up residence in an osseous microenvironment. This article outlines several notions regarding these interplays, and addresses their role in prostate carcinogenesis.