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PKC isozymes have been implicated in regulating everything from transformation and proliferation of prostate cancer cells to apoptosis. Many recent studies have implicated PKC-e, a novel PKC, in supporting cell survival and proliferation in addition to having an anti-apoptotic effect through interactions with BAX. PKC-d is another novel PKC that has been shown to promote apoptosis in LNCaP cells, and thus antagonizing the antiapoptotic effect of PKC-e. 13C-NMR and 13C(3)-aspartate supplemented media were utilized to examine the metabolism of LNCaP, DU-145 and BPH cell lines with and without activation of PKC by phorbol 12-myristate 13-acetate (PMA). Equivalent amounts of 13C-lactate were produced by the BPH cell line irrespective of addition of PMA (0.50±0.0.06 mM without PMA and 0.50±0.04 mM with PMA). The LNCaP cells produced significantly less 13C-lactate on PMA treatment from 0.40±0.04 mM to 0.25±0.10 mM, while the DU-145 cells nearly doubled the production of 13C-lactate on PMA treatment from 0.27±0.09 mM to 0.53±0.09 mM. Real-time PCR experiments showed the dramatic effect of PMA on cell metabolism could not be directly explained by the relative expression level of PKC-e and PKC-d mRNA as there was no statistically significant difference in levels of PKC-e and PKC-d mRNA. These results suggest an alternative explanation, such as 2nd messenger expression levels, need to be explored.