Carcinogenesis Advance Access published online on July 28, 2005
Carcinogenesis, doi:10.1093/carcin/bgi193
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Cancer Prevention Basic Research Project, National Cancer Center Research Institute, 1-1, Tsukiji 5-chome, Chuo-ku, Tokyo 104-0045, Japan
* To whom correspondence should be addressed. We have recently shown that the prostaglandin E2 (PGE2) receptor EP3 plays an important role in suppression of colon cancer cell proliferation and its deficiency enhances late stage colon carcinogenesis. Here we examined the effects of EP3-deficiency on two-stage skin carcinogenesis. 7,12-Dimethylbenz(
Received February 16, 2005
Revised July 16, 2005
Accepted July 22, 2005
CANCER BIOLOGY
Prostaglandin E receptor EP3 deficiency modifies tumor outcome in mouse two-stage skin carcinogenesis
2 Department of Biological Safety Research, Japan Food Research Laboratories, Bunkyo 2-3, Chitose-shi, Hokkaido 066-0052, Japan
3 Minase Research Institute, Ono Pharmaceutical Co. Ltd., 1-1, Sakurai 3-chome, Shimamoto-cho, Mishima-gunn, Osaka 606-8501, Japan
4 Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto-shi, Kyoto 606-8501, Japan
5 Department of Pharmacology, School of Medicine, Kyoto University, Kyoto-shi, Kyoto 606-8501, Japan
Keiji Wakabayashi, E-mail: kwakabay{at}gan2.res.ncc.go.jp
Abstract 
)anthracene (DMBA; 50 µg / 200 µl of acetone) was thus applied to the back skin of female EP3 knockout and wild-type mice at 8 weeks of age, followed by treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA; 5 µg / 200 µl of acetone) twice a week for 25 weeks. First tumor appearance in EP3-knockout mice was at week 10, 3 weeks later than in EP3 wild-type mice, and multiplicity at week 11 was significantly lower in the EP3-knockout case. However, histological examination showed that the tumor incidence and multiplicity at week 25 were not significantly changed in knockout mice and wild-type mice (incidence, 19/19 vs 23/24; multiplicity, 3.58 ± 0.51 vs 3.17 ± 0.63, respectively). Interestingly, there were no squamous cell carcinomas (SCCs) in the EP3 knockout mice, while SCCs were observed in 3 out of 24 wild-type mice. Furthermore, benign keratoacanthomas only developed in EP3 knockout mice (6/19 vs 0/24, P<0.01). The results suggest that PGE2 receptor EP3 signaling might contribute to development of SCCs in the skin.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  K.-S. Chun, H.-C. Lao, C. S. Trempus, M. Okada, and R. Langenbach The prostaglandin receptor EP2 activates multiple signaling pathways and {beta}-arrestin1 complex formation during mouse skin papilloma development Carcinogenesis, September 1, 2009; 30(9): 1620 - 1627. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Makita, M. Mutoh, T. Maruyama, K. Yonemoto, A. Kobayashi, H. Fujitsuka, M. Toida, T. Shibata, S. Miyamoto, Y. Yasui, et al. A prostaglandin E2 receptor subtype EP1-selective antagonist, ONO-8711, suppresses 4-nitroquinoline 1-oxide-induced rat tongue carcinogenesis Carcinogenesis, March 1, 2007; 28(3): 677 - 684. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. M. Fulton, X. Ma, and N. Kundu Targeting Prostaglandin E EP Receptors to Inhibit Metastasis. Cancer Res., October 15, 2006; 66(20): 9794 - 9797. [Abstract] [Full Text] [PDF]
|
|