Cannabinoids attenuate cancer pain and proliferation in a mouse model

被引:13
作者
Saghafi, Negin [3 ]
Lam, David K. [4 ]
Schmidt, Brian L. [1 ,2 ]
机构
[1] NYU, Bluestone Ctr Clin Res, New York, NY 10010 USA
[2] NYU, Dept Oral & Maxillofacial Surg, New York, NY 10003 USA
[3] Univ Calif San Francisco, UCSF Sch Dent, San Francisco, CA 94143 USA
[4] Univ Calif San Francisco, Dept Oral & Maxillofacial Surg, San Francisco, CA 94143 USA
关键词
Cannabinoids; Cell viability; Cancer mouse model; Cancer pain; CB1; receptor; CB2; GROWTH-FACTOR; TUMOR-GROWTH; IN-VIVO; RECEPTOR; ACTIVATION; AGONIST; HYPERALGESIA; INHIBITION; PROGRESS; THERAPY;
D O I
10.1016/j.neulet.2010.11.039
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We investigated the effects of cannabinoid receptor agonists on (1) oral cancer cell viability in vitro and (2) oral cancer pain and tumor growth in a mouse cancer model. We utilized immunohistochemistry and Western blot to show that human oral cancer cells express CBr1 and CBr2. When treated with WIN55,2122 (non-selective), ACEA (CBr1-selective) or AM1241 (CBr2-selective) agonists in vitro, oral cancer cell proliferation was significantly attenuated in a dose-dependent manner. In vivo, systemic administration (0.013 M) of WIN55,212-2, ACEA, or AM1241 significantly attenuated cancer-induced mechanical allodynia. Tumor growth was also significantly attenuated with systemic AM1241 administration. Our findings suggest a direct role for cannabinoid mechanisms in oral cancer pain and proliferation. The systemic administration of cannabinoid receptor agonists may have important therapeutic implications wherein cannabinoid receptor agonists may reduce morbidity and mortality of oral cancer. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:247 / 251
页数:5
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