MediCity Research Laboratory and InFLAMES Flagship, University of Turku, Turku, Finland (G.G.Y.); Department of Neurosurgery, Robert Wood Johnson and New Jersey Medical Schools, Rutgers University, Piscataway, New Jersey (D.B.); and Rutgers Brain Health Institute, Piscataway, New Jersey (D.B.)
Pharmacol Rev. 2022 Jul;74(3):797-822. doi: 10.1124/pharmrev.121.000528.
Adenosine is an evolutionary ancient metabolic regulator linking energy state to physiologic processes, including immunomodulation and cell proliferation. Tumors create an adenosine-rich immunosuppressive microenvironment through the increased release of ATP from dying and stressed cells and its ectoenzymatic conversion into adenosine. Therefore, the adenosine pathway becomes an important therapeutic target to improve the effectiveness of immune therapies. Prior research has focused largely on the two major ectonucleotidases, ectonucleoside triphosphate diphosphohydrolase 1/cluster of differentiation (CD)39 and ecto-5'-nucleotidase/CD73, which catalyze the breakdown of extracellular ATP into adenosine, and on the subsequent activation of different subtypes of adenosine receptors with mixed findings of antitumor and protumor effects. New findings, needed for more effective therapeutic approaches, require consideration of redundant pathways controlling intratumoral adenosine levels, including the alternative NAD-inactivating pathway through the CD38-ectonucleotide pyrophosphatase phosphodiesterase (ENPP)1-CD73 axis, the counteracting ATP-regenerating ectoenzymatic pathway, and cellular adenosine uptake and its phosphorylation by adenosine kinase. This review provides a holistic view of extracellular and intracellular adenosine metabolism as an integrated complex network and summarizes recent data on the underlying mechanisms through which adenosine and its precursors ATP and ADP control cancer immunosurveillance, tumor angiogenesis, lymphangiogenesis, cancer-associated thrombosis, blood flow, and tumor perfusion. Special attention is given to differences and commonalities in the purinome of different cancers, heterogeneity of the tumor microenvironment, subcellular compartmentalization of the adenosine system, and novel roles of purine-converting enzymes as targets for cancer therapy. SIGNIFICANCE STATEMENT: The discovery of the role of adenosine as immune checkpoint regulator in cancer has led to the development of novel therapeutic strategies targeting extracellular adenosine metabolism and signaling in multiple clinical trials and preclinical models. Here we identify major gaps in knowledge that need to be filled to improve the therapeutic gain from agents targeting key components of the adenosine metabolic network and, on this basis, provide a holistic view of the cancer purinome as a complex and integrated network.
腺苷是一种古老的代谢调节剂,将能量状态与生理过程(包括免疫调节和细胞增殖)联系起来。肿瘤通过死亡和应激细胞中 ATP 的释放增加及其在外切酶作用下转化为腺苷,从而产生富含腺苷的免疫抑制微环境。因此,腺苷途径成为改善免疫治疗效果的重要治疗靶点。先前的研究主要集中在两种主要的外核苷酸酶,即外核苷酸三磷酸二磷酸水解酶 1/分化群(CD)39 和外 5'-核苷酸酶/CD73,它们催化细胞外 ATP 分解为腺苷,以及随后激活不同亚型的腺苷受体,其抗肿瘤和促肿瘤作用的研究结果喜忧参半。需要考虑控制肿瘤内腺苷水平的冗余途径,包括通过 CD38-外核苷酸焦磷酸酶磷酸二酯酶(ENPP)1-CD73 轴的替代 NAD 失活途径、拮抗的 ATP 再生外切酶途径以及细胞内腺苷摄取及其由腺苷激酶磷酸化等新发现,这需要更有效的治疗方法,这些新发现需要考虑控制肿瘤内腺苷水平的冗余途径,包括通过 CD38-外核苷酸焦磷酸酶磷酸二酯酶(ENPP)1-CD73 轴的替代 NAD 失活途径、拮抗的 ATP 再生外切酶途径以及细胞内腺苷摄取及其由腺苷激酶磷酸化等新发现,这需要更有效的治疗方法,这些新发现需要考虑控制肿瘤内腺苷水平的冗余途径,包括通过 CD38-外核苷酸焦磷酸酶磷酸二酯酶(ENPP)1-CD73 轴的替代 NAD 失活途径、拮抗的 ATP 再生外切酶途径以及细胞内腺苷摄取及其由腺苷激酶磷酸化等新发现,这需要更有效的治疗方法,这些新发现需要考虑控制肿瘤内腺苷水平的冗余途径,包括通过 CD38-外核苷酸焦磷酸酶磷酸二酯酶(ENPP)1-CD73 轴的替代 NAD 失活途径、拮抗的 ATP 再生外切酶途径以及细胞内腺苷摄取及其由腺苷激酶磷酸化等新发现,这需要更有效的治疗方法,这些新发现需要考虑控制肿瘤内腺苷水平的冗余途径,包括通过 CD38-外核苷酸焦磷酸酶磷酸二酯酶(ENPP)1-CD73 轴的替代 NAD 失活途径、拮抗的 ATP 再生外切酶途径以及细胞内腺苷摄取及其由腺苷激酶磷酸化等新发现,这需要更有效的治疗方法,这些新发现