According to the World Health Organization,
bladder cancer is the seventh most common
cancer among men in the world. The current treatments for this
malignancy are not efficient to prevent the recurrence and progression of
tumors. Then, researches continue looking for better therapeutic targets which can end up in new and more efficient treatments. One of the recent findings was the identification that the purinergic system was involved in bladder
tumorigenesis. The ectonucleotidases, mainly
ecto-5'-nucleotidase/CD73 have been revealed as new players in
cancer progression and malignity. In this work, we investigated the NTPDase3 and
ecto-5'-nucleotidase/CD73 expression in
cancer progression in vivo.
Bladder tumor was induced in mice by the addition of 0.05 % of N-butyl-N-(hydroxybutyl)-
nitrosamine (BBN) in the
drinking water for 4, 8, 12, 18, and 24 weeks. After this period, mice bladders were removed for histopathology analysis and immunofluorescence assays. The bladder of animals which has received BBN had alterations, mainly
inflammation, in initial times of
tumor induction. After 18 weeks, mice's bladder has developed histological alterations similar to human
transitional cell carcinoma. The cancerous urothelium, from mice that received BBN for 18 and 24 weeks, presented a weak immunostaining to NTPDase3, in contrast to an increased expression of
ecto-5'-nucleotidase/CD73. The altered expression of NTPDase3 and
ecto-5'-nucleotidase/CD73 presented herein adds further evidence to support the idea that alterations in ectonucleotidases are involved in bladder
tumorigenesis and reinforce the
ecto-5'-nucleotidase/CD73 as a future
biomarker and/or a target for pharmacological
therapy of
bladder cancer.