The role of the renin-angiotensin system (RAS) in the development of various malignancies has recently been extensively examined and, since it has been shown to significantly influence many aspect of cancer initiation and progression, the idea of RAS-targeted anticancer therapy has arisen. This article reviews the mechanisms underlying RAS-induced physiological and pathological responses related to cancer biology, including tumor growth, cell proliferation, apoptosis, angiogenesis, inflammation, and protein degradation, emphasizing the associated cellular transduction schemes activated by main RAS effectors. Also the dual nature of RAS-dependent effects, resulting from its complex physiology has been commented. Finally, based on the available data from clinical trials and experimental studies, the possibilities of the introduction of RAS-modulating drugs into standard clinical practice in oncology have been discussed with the focus on both, positive and negative effects associated with the administration of various classes of pharmaceuticals to cancer patients.