| First Author | Johnson DT | Year | 2013 |
| Journal | J Biol Chem | Volume | 288 |
| Issue | 6 | Pages | 3727-38 |
| PubMed ID | 23275340 | Mgi Jnum | J:196012 |
| Mgi Id | MGI:5486402 | Doi | 10.1074/jbc.M112.417568 |
| Citation | Johnson DT, et al. (2013) Deletion of leucine zipper tumor suppressor 2 (Lzts2) increases susceptibility to tumor development. J Biol Chem 288(6):3727-38 |
| abstractText | Using an Lzts2 knock-out mouse model, we characterized the biological role of Lzts2 in tumorigenesis. Both heterozygous and homozygous deletion of the Lzts2-targeted allele in mice shows an increased incidence in spontaneous tumor development, although Lzts2 homozygous knock-out mice show significantly higher incidences than heterozygous mice. Treatment of Lzts2-deficient mice with a carcinogen, N-butyl-N-(4-hydroxybutyl) nitrosamine, increases the susceptibility to N-butyl-N-(4-hydroxybutyl) nitrosamine-induced bladder carcinoma development. Examination of human prostate cancer tissue specimens shows a reduction of LZTS2 protein expression in prostate cancer cells. Further analyses of mouse embryonic fibroblasts isolated from Lzts2 knock-out embryos show that loss of Lzts2 enhances cell growth. These data provide the first line of evidence demonstrating that deletion of Lzts2 increases susceptibility to spontaneous and carcinogen-induced tumor development. |
