Mice deficient for Lgr4 are resistant to TPA-induced keratinocyte proliferation and onset of papillomas.
TPA treatment activated MEK1/ERK1/2/AP-1 and Wnt/β-catenin signaling pathways in vitro and in vivo in wild-type but not Lgr4−/− mice.
We provide evidence that MEK1/ERK1/2 pathway activation lies upstream of Wnt/β-catenin pathway activation during mouse skin tumor formation.