Key result
Adiponectin reduces prostate cancer cell proliferation, an effect leptin blocks via altered ERK signaling.
Adiponectin reduces prostate cancer cell proliferation, an effect that can be blocked by leptin via the ERK pathway, suggesting a role for these hormones in prostate cancer.
Should not yet influence prostate cancer management; leaves open adiponectin-leptin-ERK interactions for preclinical study.
We hypothesize that adiponectin and leptin may be capable of mediating some of the effects that body weight has on prostate cancer and that a mouse model may be effective to examine this hypothesis. We found that tumors from the TRAMP prostate cancer model expressed adiponectin and leptin receptors. TRAMP-C2 prostate cancer cell proliferation was reduced by adiponectin. Leptin was able to block the ability of adiponectin to reduce cell proliferation through altered signaling of the ERK pathway. Overall, this work suggests that adiponectin, leptin, and their receptors may play an important role in prostate cancer.
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Grossmann et al. (2009) studied Prostate cancer. Adiponectin and leptin was evaluated on Cell proliferation and receptor expression. Adiponectin reduced TRAMP-C2 prostate cancer cell proliferation, an effect that was blocked by leptin through altered signaling of the ERK pathway.
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