期刊
CANCER RESEARCH
卷 75, 期 4, 页码 635-644出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-14-1259
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资金
- AIRC [IG 5354, IG 14442]
- Telethon [GGP06070]
- ERA-NET Neuron Nanostroke
- Ministry of Health of Italy [RF-2011-02348435]
- Italian Ministry of Education, University and Research [RBAP11FXBC_001]
- University of Ferrara
- 7th Framework Program ATPBone [HEALTH-F2-2007-202231]
- Italian Ministry of Education, University and Research (COFIN) [20129JLHSY_002]
- Italian Ministry of Education, University and Research (FIRB) [RBAP11FXBC_002]
- Italian Ministry of Education, University and Research (Futuro in Ricerca) [RBFR10EGVP_001]
- My First AIRC Grant (MFAG) [11630]
- Young Investigator Grant Alessandro Liberati from Regione Emilia-Romagna
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-1 beta 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. (C)2014 AACR.
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