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FEZ1/LZTS1  is a tumor suppressor gene that is frequently altered in human cancers of different histotypes. We have reported previously that   LZTS1  is downregulated in high-grade bladder cancer and that its restoration suppresses tumorigenicity in urothelial carcinoma cells. To further investigate the role of   LZTS1  in the development of bladder cancer, we utilized heterozygous and nullizygous   Lzts1  mice in a chemically induced carcinogenesis model. Fifty-eight mice consisting of 25   Lzts1  +/+  , 17   Lzts1  +/−  and 16   Lzts1  −/−  were treated with   N  -butyl-  N  -(4-hydroxybutil) nitrosamine (BBN). Results showed that there was a significant increase in neoplastic lesions in the   Lzts1  +/−  (82.3%) and   Lzts1  −/−  (93.8%) versus   Lzts1  +/+  (8.0%) mice after BBN treatment. No difference in cancer incidence between   Lzts1  +/−  and   Lzts1  −/−  was observed. Collectively, these findings indicate that loss of one or both   LZTS1  alleles hampers the normal defenses of urothelial cells against carcinogens, favoring bladder cancer development. Therefore,   LZTS1  may become an excellent target for gene therapy in advanced bladder carcinoma.

Fez1/Lzts1 -deficient mice are more susceptible to N -butyl- N -(4-hydroxybutil) nitrosamine (BBN) carcinogenesis