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Effects of angiotensin II on mitochondrial physiology in normal (PWR‐1E) and malignant (LNCaP) prostate epithelium cell lines

Prostate cancer is diagnosed in over 186,000 men in the United States and accounts for more than 28,000 deaths annually. The epidemiology of prostate cancer is identified by risk factors including genetics, diet, smoking alcohol consumption, chronic inflammation, hypertension and age. Angiotensen II (AngII) is a major effector peptide of the rennin‐angiotensin system (RAS), and is an important factor in hypertension. RAS interacts with the autocrine/paracrine system, and relates to cell growth and differentiation in some organs. Investigators have reported that exogenous application of Ang II to LNCaP cells results in the activation of Akt signaling, increased activity of SOD, and glutathione peroxidase. Another common characteristic of tumor cells is the shift away from oxidative phosphorylation to a conversion of pyruvate to lactate in the presence of ample oxygen, it remains unclear whether “aerobic glycolysis” is cause, effect, or either depending on the cancer under study. We investigated the effects of Ang II in a non‐malignant and malignant prostate cell line in order to document effects of Ang II specific to mitochondrial bioenergetics in a cancer phenotype. Our results suggest that aerobic glycolysis is induced in both cell lines, but is mediated by disparate signaling pathways.