Targeting estrogen receptor-β for the prevention of nonmelanoma skin cancer.
The potential for targeting estrogen receptor (ER)-β in various cancer models has been gaining considerable attention in recent years. In this issue of the journal, Chaudhary and colleagues demonstrate markedly decreased ultraviolet B (UVB)-induced skin cancer in a mouse model using a highly specific ER-β agonist, ERB-041. The mechanisms that underlie this strong inhibitory effect are mediated by inhibition of proinflammatory signaling and epithelial-mesenchymal transition (EMT). The changes in EMT were due in part to modulation of WNT/β-catenin signaling. Collectively, the results from these studies provide important new insights into the mechanisms by which the ER-β agonist ERB-041 inhibits UVB-induced skin cancer and opens the door for future studies that could examine combinatorial approaches for UVB-dependent skin cancer chemoprevention.
Department of Veterinary and Biomedical Sciences and Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, Life Sciences Building, University Park, PA 16802. jmp21@psu.edu.
Pei-Li
PL
Yao
Frank J
FJ
Gonzalez
Jeffrey M
JM
Peters
D000818:Animals; D063646:Carcinogenesis / Q000187:drug effects*; D005260:Female; D006801:Humans; D010080:Oxazoles / Q000494:pharmacology*; D012878:Skin Neoplasms / Q000517:prevention & control*; D060449:Wnt Signaling Pathway / Q000187:drug effects*
C478102:ERB 041; D010080:Oxazoles