Krüppel-like factor 10 (KLF10) has been suggested to be a putative tumor 
suppressor. In the present study, we generated KLF10 deficient mice to explore 
this hypothesis in vivo. KLF10 deficient mice exhibited increased predisposition 
to skin tumorigenesis and markedly accelerated papilloma development after 
DMBA/TPA treatment. On the other hand, KLF10 deficient keratinocytes showed 
increased proliferation and apoptosis. In colony formation assays after 
oncogenic H-Ras transfection, KLF10 deficient mouse embryonic fibroblasts (MEFs) 
yielded more colonies than wild-type MEFs. Furthermore, KLF10 dose-dependently 
activated p21(WAF1/CIP1) transcription, which was independent of p53 and Sp1 
binding sites in p21(WAF1/CIP1) promoter. This study demonstrates that KLF10 is 
a tumor suppressor and that it targets p21(WAF1/CIP1) transcription.