evaluating the expression of bmi-1, as a new molecular marker in diagnosis and classification of bladder tumors

objectives: tissue homeostasis is the result of strict regulatory mechanisms, which control self-renewal, differentiation, prevention of premature senescence and apoptosis of stem cells. bmi-1, a polycomb group repressor protein, represses genes that induce cellular senescence and cell death, and can contribute to cancer when improperly expressed. material and methods: bladder tumoral and nontumoral samples were collected from labbafi-nejad hospital. rna was extracted from each sample, reverse transcribed and amplified by rt-pcr technique, using specific primers for bmi-1 and β2-microglobolin, as an internal control. the production and distribution of bmi-1 protein was also examined by western blotting and immunohistochemistry technique. results: to clarify the role of bmi-1 in bladder tumors, we examined the expression of bmi-1 in tumoral and nontumoral samples. rt-pcr generated a 683 bp product, corresponding to the expected size of the bmi-1 amplified region. the identity of the amplified fragment was then confirmed by direct dna sequencing. the mean of expression of the bmi-1 detected in tumoral tissues was significantly higher than the non-tumoral tissues and there is also a significant correlation between the mean of gene expression with stage of malignancy (p < 0.05). the expression of bmi-1 at protein level was further confirmed by western blotting and immunohistochemistry. conclusion: the tumor suppressor locus cdkn2a (ink4a/arf locus) codes for two proteins, p16ink4a and p14arf. ink4a and arf are playing important roles in the retinoblastoma (prb) and p53 pathways, respectively. bmi-1 is a potent repressor of both pathways and hence elucidating its role in tumorigenisis is very important. here, for the first time we are reporting the expression of bmi-1 and its correlation with malignancy in bladder tumors.