G-protein-coupled receptors (GPCRs) are the largest and most diverse group of cellular membrane receptors identified and characterized. It is estimated that 30 to 50% of marketed drugs target these receptors. The angiotensin II receptor type 1 (AT1R) is a GPCR which signals in response to systemic alterations of the peptide hormone angiotensin II (AngII) in circulation. The enzyme responsible for converting AngI to AngII is the angiotensin-converting enzyme (ACE). Specific inhibitors for the AT1R (more commonly known as AT1R blockers or antagonists) and ACE are well characterized for their effects on the cardiovascular system. Combined with the extensive clinical data available on patient tolerance of AT1R blockers (ARBs) and ACE inhibitors (ACEIs), as well as their non-classical roles in cancer, the notion of repurposing this class of medications as cancer treatment(s) is explored in the current review. Given that AngII-dependent AT1R activity directly regulates angiogenesis, remodeling of vasculature, pro-inflammatory responses, stem cell programming and hematopoiesis, and electrolyte balance; the modulation of these processes with pharmacologically well characterized medications could present a valuable complementary treatment option for cancer patients.

G蛋白偶联受体（GPCR）是鉴定和表征的最大，最多样化的细胞膜受体。据估计，市售药物的30％至50％靶向这些受体。1型血管紧张素II受体（AT1R）是一种GPCR，可响应循环中肽激素血管紧张素II（AngII）的系统性变化发出信号。负责将AngI转换为AngII的酶是血管紧张素转换酶（ACE）。针对AT1R的特定抑制剂（通常称为AT1R阻断剂或拮抗剂）和ACE对心血管系统的作用已得到很好的表征。结合有关AT1R阻断剂（ARB）和ACE抑制剂（ACEI）的患者耐受性及其在癌症中的非经典作用的广泛临床数据，在本综述中，探讨了将此类药物重新用作癌症治疗的概念。鉴于依赖AngII的AT1R活性直接调节血管生成，血管系统重塑，促炎反应，干细胞编程和造血作用以及电解质平衡；用药理学特征明确的药物调节这些过程可能为癌症患者提供有价值的补充治疗选择。