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Mitochondria are key organelles for ATP production and apoptosis. Therefore, impairment of mitochondria can modulate or accelerate cancer progression. p32, originally identified as a pre-mRNA splicing factor SF2/ASF-associated protein, is localized predominantly in the mitochondrial matrix and involved in mitochondria respiration. Recently, p32 was implicated in apoptosis and resultantly cancer progression. However, little is known about the expression and function of p32 in human tumors including prostate cancer. Here, we investigated the expression of p32 in 148 prostate carcinoma tissues by immunohistochemistry and found a positive correlation of p32 expression to clinicopathological parameters including follow-up data. p32 is highly expressed in prostate tumor samples and its expression is significantly associated with the Gleason score, pathological stage and relapse. For localized cancers, high p32 is a strong and independent predictor of clinical recurrence in multivariate analysis (P=0.01). In addition, p32 is overexpressed in the prostate cancer cell lines examined. The selective knockdown of p32 by RNA interference inhibits the growth of prostate cancer cell lines but not of a non-cancerous cell line. The p32 RNA interference decreases cyclin D1, increases p21 expression and causes a G1/S cell cycle arrest in prostate cancer cells. These data suggest that p32 is critical for prostate cancer cell proliferation and may be a novel marker of clinical progression in prostate cancer., (© 2011 Japanese Cancer Association.)

Prostate specific antigen(PSA) is widely used as a marker for screening and monitoring prostate cancer. However, there are several assay methods, which often give different PSA values for the same patient sample. A possible cause of these discrepancies might be the varied immunoreactivity with free-PSA and complex-PSA among methods. This study revealed that pre-treatment of samples with anti-free-PSA monoclonal antibodies improved polyclonal antibodies-based non equimolar PSA assay to equimolar assay. This might be achieved by that the monoclonal antibodies bind to free-PSA and then change its reactivities with polyclonal antibodies to those similar to complex-PSA.