Effects of Metformin and Combinatory Derived Factors of Adipose Tissue on Prostate Cancer Growth
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Abstract
Obesity is a growing concern worldwide and is associated with increased risk of prostate cancer (PCa) and poor patient prognosis. Metformin (MET) is reported to be protective against PCa in type 2 diabetics as they are at a reduced risk of developing PCa and have a better prognosis if they do in fact develop PCa. My thesis examined the effects of MET on two prostate cancer cell lines, LNCaP and PC3 cells. MET caused alterations in morphology and cell detachment in both cell lines. MET counteracted the effects of leptin which was independent of AMPK activation. PC3 cells incubation with conditioned media and treated with MET caused increased AMPK activation and decreased AKT activation. MET was found to act independently of AMPK although it caused an increase in AMPK activation in PC3 cells. It appears that MET represents a promising adjuvant therapy for obese PCa patients.