TY - JOUR
T1 - Protective effect of hyperpigmented skin on UV-mediated cutaneous cancer development
AU - Kato, Masashi
AU - Ohgami, Nobutaka
AU - Kawamoto, Yoshiyuki
AU - Tsuzuki, Toyonori
AU - Hossain, Khaled
AU - Yanagishita, Takeshi
AU - Ohshima, Yuichiro
AU - Tsuboi, Hideo
AU - Yamanoshita, Osamu
AU - Matsumoto, Yoshinari
AU - Takahashi, Masahide
AU - Nakashima, Izumi
N1 - Funding Information:
This study was supported in part by Grants-in-Aid for Scientific Research (B) (16310037) and (c) (18590578), Grant-in-Aid for Young Scientists (B) (18790738) and Grant-in-Aid for Exploratory Research (17659344) from the Ministry of Education, Culture, Sports, Science and Technology (MEXT), Grant-in Aid for JSPS Fellows from Japan Society for the Promotion of Science (JSPS) (P05444), a Grant for the Basic Dermatological Research from Shiseido Co. Ltd, the Cosmetology Research Foundation, the Tokyo Biochemical Research Foundation (TBRF) Postdoctoral fellowship for Asian Researcher, the Uehara Memorial Foundation Research Grant, and the Sasakawa Scientific Research Grant from the Japan Science Society. We thank Kozo Uchiyama, Yoko Kato, Kyoko Ohgami, and Shizuka Tajima for technical assistance.
PY - 2007/5
Y1 - 2007/5
N2 - Recently, we crossed an original haired RET-transgenic mouse of line 242 with a hairless mouse and established a hairless RET-(HL/RET)-transgenic mouse line (242-hr/hr) with hyperpigmented skin but no tumors. In this study, we examined the effect of hyperpigmented skin in HL/RET-transgenic mice on UV irradiation-mediated cutaneous cancer development. UV irradiation to this mouse line never induced melanoma despite the presence of melanoma-inducible transgenic RET oncogenes. On the contrary, the hyperpigmented skin efficiently protected UV-mediated squamous carcinoma development in the skin. Probably underlying this result, hyperpigmentation protected the skin from damage and blocked the accompanying signal transduction for tyrosine phosphorylation of multiple cellular proteins and activation/phosphorylation of extracellular signal-regulated, c-Jun N-terminal, and p38 kinases. Thus, we demonstrated hyperpigmentation-mediated in vivo protection against UV irradiation-induced skin cancer.
AB - Recently, we crossed an original haired RET-transgenic mouse of line 242 with a hairless mouse and established a hairless RET-(HL/RET)-transgenic mouse line (242-hr/hr) with hyperpigmented skin but no tumors. In this study, we examined the effect of hyperpigmented skin in HL/RET-transgenic mice on UV irradiation-mediated cutaneous cancer development. UV irradiation to this mouse line never induced melanoma despite the presence of melanoma-inducible transgenic RET oncogenes. On the contrary, the hyperpigmented skin efficiently protected UV-mediated squamous carcinoma development in the skin. Probably underlying this result, hyperpigmentation protected the skin from damage and blocked the accompanying signal transduction for tyrosine phosphorylation of multiple cellular proteins and activation/phosphorylation of extracellular signal-regulated, c-Jun N-terminal, and p38 kinases. Thus, we demonstrated hyperpigmentation-mediated in vivo protection against UV irradiation-induced skin cancer.
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U2 - 10.1038/sj.jid.5700659
DO - 10.1038/sj.jid.5700659
M3 - Article
C2 - 17159911
AN - SCOPUS:34247249893
VL - 127
SP - 1244
EP - 1249
JO - Journal of Investigative Dermatology
JF - Journal of Investigative Dermatology
SN - 0022-202X
IS - 5
ER -