biostudies-literatureJohnson DTNCI NIH HHS3727-38https://www.ebi.ac.uk/biostudies/studies/S-EPMC3567628biostudies-literatureUnknown288(6)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.The Journal of biological chemistryDeletion of leucine zipper tumor suppressor 2 (Lzts2) increases susceptibility to tumor development.PMC3567628CA-070297CA-151623R01 CA070297R01 CA151623R29 CA070297Luong RPeng YShaltouki AJohnson DTLee JTLin DLee SHWang YSun ZfalseDeletion of leucine zipper tumor suppressor 2 (Lzts2) increases susceptibility to tumor development.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.2013-01-01T00:00:00Z2013 Feb2021-02-28T08:22:03Z2019-03-27T01:04:32ZS-EPMC35676282327534010.1074/jbc.m112.41756810.1074/jbc.M112.417568