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.