In previous studies we have reported that a high levelof expression of mot-2 protein results in malignant transformation of NIH 3T3 cells as analyzed by anchorage indeopendent growth and nude mice assays [Kaul et al....In previous studies we have reported that a high levelof expression of mot-2 protein results in malignant transformation of NIH 3T3 cells as analyzed by anchorage indeopendent growth and nude mice assays [Kaul et al., Oncogene, 17, 907-11, 1998]. Mot-2 was found to interact withtumor suppressor protein p53. The transient overexpression of mot-2 was inhibitory to transcriptional activationfunction of p53 [Wadhwa et al., J. Biol. Chem., 273, 2958691, 1998]. We demonstrate here that mot-2 transfectedstable clonse of NIH 3T3 that showed malignant propertiesindeed show inactivation of p53 function as assayed byexogenous p53 dependent reporter. The expression levelof p53 in response to UV-irradiation was lower in NIH3T3/mot-2 as compared to NIH 3T3 cells and also exhibited delay in reaching peak. furthermore, upon serumstarvation p53 was seen to translocate to the 11ucleus inNIH 3T3, but not in its mot-2 derivative. The data suggests that mot-2 mediated cytoplasmic sequestration andinactivation of p53 may operate, at least in part, for malignant phenotype of NIH 3T3/mot-2 cells.NIH 3T3/mot-2 cells show inactivation of p53 protein展开更多
文摘In previous studies we have reported that a high levelof expression of mot-2 protein results in malignant transformation of NIH 3T3 cells as analyzed by anchorage indeopendent growth and nude mice assays [Kaul et al., Oncogene, 17, 907-11, 1998]. Mot-2 was found to interact withtumor suppressor protein p53. The transient overexpression of mot-2 was inhibitory to transcriptional activationfunction of p53 [Wadhwa et al., J. Biol. Chem., 273, 2958691, 1998]. We demonstrate here that mot-2 transfectedstable clonse of NIH 3T3 that showed malignant propertiesindeed show inactivation of p53 function as assayed byexogenous p53 dependent reporter. The expression levelof p53 in response to UV-irradiation was lower in NIH3T3/mot-2 as compared to NIH 3T3 cells and also exhibited delay in reaching peak. furthermore, upon serumstarvation p53 was seen to translocate to the 11ucleus inNIH 3T3, but not in its mot-2 derivative. The data suggests that mot-2 mediated cytoplasmic sequestration andinactivation of p53 may operate, at least in part, for malignant phenotype of NIH 3T3/mot-2 cells.NIH 3T3/mot-2 cells show inactivation of p53 protein
