The Cannabinoid Receptors Are Required for Ultraviolet-Induced Inflammation and Skin Cancer Development

Zheng, Duo; Bode, Ann M.; Zhao, Qing; Cho, Yong‐Yeon; Zhu, Feng; Ya, Wei; Dong, Zigang

doi:10.1158/0008-5472.can-07-6594

Cited by 89 publications

(84 citation statements)

References 47 publications

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“…To achieve wrinkle removal by dermal remodeling, inflammatory process is accompanied [2]. Repeated tissue damage coupled with chronic inflammation can stimulate carcinogenesis [8].…”

Section: Introductionmentioning

confidence: 99%

Preventive effect of chemical peeling on ultraviolet induced skin tumor formation

Abdel-Daim

Funasaka

Kamo

et al. 2010

Journal of Dermatological Science

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“…To achieve wrinkle removal by dermal remodeling, inflammatory process is accompanied [2]. Repeated tissue damage coupled with chronic inflammation can stimulate carcinogenesis [8].…”

Section: Introductionmentioning

confidence: 99%

Preventive effect of chemical peeling on ultraviolet induced skin tumor formation

Abdel-Daim

Funasaka

Kamo

et al. 2010

Journal of Dermatological Science

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“…1 UVBinduced skin inflammatory reactions constitute a potent tumor-promoting event that contributes to photocarcinogenesis. [14][15][16] Thus, development of a method for regulating UVB-induced acute effects is important for protection against photocarcinogenesis. However, the molecular mechanisms by which UVB induces acute effects on the skin have not been fully clarified.…”

mentioning

confidence: 99%

Phospholipase Cɛ has a crucial role in ultraviolet B-induced neutrophil-associated skin inflammation by regulating the expression of CXCL1/KC

Oka

Edamatsu

Kunisada

et al. 2011

Laboratory Investigation

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Phospholipase C (PLC) e is a phosphoinositide-specific PLC regulated by small GTPases including Ras and Rap. We previously demonstrated that PLCe has an important role in the development of phorbol ester-induced skin inflammation. In this study, we investigated the role of PLCe in ultraviolet (UV) B-induced acute inflammatory reactions in the skin. Wild-type (PLCe þ / þ ) and PLCe gene knockout (PLCe À/À ) mice were irradiated with a single dose of UVB at 1, 2.5, and 10 kJ/m 2 on the dorsal area of the skin, and inflammatory reactions in the skin were histologically evaluated up to 168 h after irradiation. In PLCe þ / þ mice, irradiation with 1 and 2.5 kJ/m 2 UVB resulted in dose-dependent neutrophil infiltration in the epidermis at 24 and 48 h after irradiation. When mice were irradiated with 10 kJ/m 2 of UVB, most mice developed skin ulcers by 48 h and these ulcers became more severe at 168 h. In PLCe À/À mice, UVB (1 or 2.5 kJ/m 2 )-induced neutrophil infiltration was markedly suppressed compared with PLCe þ / þ mice. The suppression of neutrophil infiltration in PLCe À/À mice was accompanied by attenuation of UVB-induced production of CXCL1/keratinocyte-derived chemokine (KC), a potent chemokine for neutrophils, in the whole skin. Cultured epidermal keratinocytes and dermal fibroblasts produced CXCL1/KC in a PLCe-dependent manner after UVB irradiation, and the UVB-induced upregulation of CXCL1/KC in these cells was significantly abolished by a PLC inhibitor. Furthermore, UVB-induced epidermal thickening was noticeably reduced in the skin of PLCe À/À mice. These results indicate that PLCe has a crucial role in UVB-induced acute inflammatory reactions such as neutrophil infiltration and epidermal thickening by at least in part regulating the expression of CXCL1/KC in skin cells such as keratinocytes and fibroblasts.

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“…Of note, both the CB1 and CB2 receptors seem to play a key role in UV-induced inflammation and skin cancer development [Zheng et al, 2008]. The involvement of NK cells in these observations remains to be studied.…”

Section: An Endocannabinoid Connection?mentioning

confidence: 99%

Cancer therapeutics: reflections on natural killer cells

Genevieve

2008

Drug Development Research

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Cancer remains a leading cause of death globally, including in developing countries. In spite of the introduction of several new drugs to the anti-cancer arsenal in recent years, including monoclonal antibodies and selective tyrosine kinase inhibitors blocking the action of cancer-promoting hormones, full remission remains exceptional in many common cancers including lung, pancreas, and stomach cancers. One aspect of cancer therapeutics that remains mostly neglected is developing drugs for promoting the capacity of the innate immune system, most notably the natural killer cells, to recognize and destroy cancer cells. Minimizing the inhibition of natural killer cells' cytotoxic activity by current cancer therapeutics also deserves further consideration in cancer research. Better understanding of the physiology of the immune cells, in particular of factors regulating the action and differentiation of natural killer cells and their migration into tumor tissues, seems worthy of more in-depth research toward developing new cancer drugs. In this context, the potential of selective cannabinoid receptor agonists and fatty acid amid hydrolase inhibitors as immune-enhancing drugs deserves extra attention. Drug Dev Res 69 : 285-288, 2008.

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The Cannabinoid Receptors Are Required for Ultraviolet-Induced Inflammation and Skin Cancer Development

Cited by 89 publications

References 47 publications

Preventive effect of chemical peeling on ultraviolet induced skin tumor formation

Preventive effect of chemical peeling on ultraviolet induced skin tumor formation

Phospholipase Cɛ has a crucial role in ultraviolet B-induced neutrophil-associated skin inflammation by regulating the expression of CXCL1/KC

Cancer therapeutics: reflections on natural killer cells

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