癌症研究
免疫系统
炎症
造血
生物
骨髓
黑色素瘤
趋化性
体内
免疫
受体
原发性肿瘤
转移
癌症
免疫学
干细胞
细胞生物学
生物技术
生物化学
遗传学
作者
Elena Adinolfi,Marina Capece,Alessia Franceschini,Simonetta Falzoni,Anna Lisa Giuliani,Alessandra Rotondo,Alba Clara Sarti,Massimo Bonora,Susanne Syberg,Domenica Corigliano,Paolo Pinton,Niklas Rye Jørgensen,Luigi Abelli,Laura Emionite,Lizzia Raffaghello,Vito Pistoia,Francesco Di Virgilio
出处
期刊:Cancer Research
[American Association for Cancer Research]
日期:2014-12-27
卷期号:75 (4): 635-644
被引量:144
标识
DOI:10.1158/0008-5472.can-14-1259
摘要
Abstract The ATP receptor P2X7 (P2X7R or P2RX7) has a key role in inflammation and immunity, but its possible roles in cancer are not firmly established. In the present study, we investigated the effect of host genetic deletion of P2X7R in the mouse on the growth of B16 melanoma or CT26 colon carcinoma cells. Tumor size and metastatic dissemination were assessed by in vivo calliper and luciferase luminescence emission measurements along with postmortem examination. In P2X7R-deficient mice, tumor growth and metastatic spreading were accelerated strongly, compared with wild-type (wt) mice. Intratumoral IL-1β and VEGF release were drastically reduced, and inflammatory cell infiltration was abrogated nearly completely. Similarly, tumor growth was also greatly accelerated in wt chimeric mice implanted with P2X7R-deficient bone marrow cells, defining hematopoietic cells as a sufficient site of P2X7R action. Finally, dendritic cells from P2X7R-deficient mice were unresponsive to stimulation with tumor cells, and chemotaxis of P2X7R-less cells was impaired. Overall, our results showed that host P2X7R expression was critical to support an antitumor immune response, and to restrict tumor growth and metastatic diffusion. Cancer Res; 75(4); 635–44. ©2014 AACR.
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