AMD3100 protects from UV-induced skin cancer

被引：12

作者：

Byrne, Scott N. ^{[1
,2
,3
]}

Sarchio, Seri N. E. ^{[1
,2
,3
,4
]}

机构：

[1] Univ Sydney, Sydney Med Sch, Cellular Photoimmunol Grp, Discipline Infect Dis & Immunol, Sydney, NSW, Australia

[2] Royal Prince Alfred Hosp, Dept Dermatol, Camperdown, NSW 2050, Australia

[3] Univ Sydney, Sydney Med Sch, Bosch Inst, Discipline Dermatol, Sydney, NSW 2006, Australia

[4] Univ Putra Malaysia, Fac Med & Hlth Sci, Serdang 43400, Malaysia

来源：

ONCOIMMUNOLOGY | 2014年 / 3卷 / 01期

关键词：

chemokines; mast cells; skin cancer; immunosuppression; sunlight; ultraviolet radiation; ULTRAVIOLET-B; IRRADIATION; SUPPRESSION;

D O I：

10.4161/onci.27562

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Sunlight causes skin cancer by directly damaging DNA as well as by suppressing antitumor immune responses. A major mechanism whereby sunlight exerts immunosuppressive effects is by modulating the migration of chemokine (C-X-C motif) receptor 4 (CXCR4)-expressing dermal mast cells into and away from the skin. We have demonstrated the importance of this by showing that the systemic administration of the CXCR4 antagonist AMD3100 prevents sunlight-induced immunosuppression as well as the consequent carcinogenic response. Our results highlight the therapeutic potential of antagonizing CXCR4 signaling, especially in individuals who are at high risk of developing skin cancer.

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页数：3

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