Study on molecular carcinogenesis in transient amplifying cell of human prostate

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Transient amplifying (TA) cells are a subset of basal cell populations within the prostate from which cancers are thought to originate. Most TA cell populations showed increased expression of p53, p21, p16, and pRb, resulting in senescence. However, TA cell clones with reduced p16 expression successfully bypassed this phase. The close correlation was found between the levels of junB and p16 expression. Transfection of junB siRNA in prostatic TA cells allowed the cells to escape senescence, presumably through inactivation of p16/pRb ; this suggests that activation of junB/p16/pRb is required to block clonal expansion. Interestingly, the percentage of peripheral zone TA cells evading senescence was significantly higher than those from central and transition zones. Metastatic prostate tumors, as well as prostate cancers with high Gleason scores, demonstrated significantly low junB immunopositivity. junB thus apparently plays an important role in controlling prostate carcinogenesis and may be a new target for cancer prevention and therapy.