Researchers Gain Insights Into Mechanisms Behind Prostate Cancer Development

Researchers Gain Insights Into Mechanisms Behind Prostate Cancer Development
shutterstock_213951757A new study entitled “Loss of SIRT1 Promotes Prostatic Intraepithelial Neoplasia, Reduces Mitophagy and Delays PARK2 Translocation to Mitochondria” showed the histone deacytylase SIRT1 acts as a tumor suppressor and inhibits the formation of early prostate cancer in mice. The research was published in The American Journal of Pathology. Prostate cancer is currently the second leading cause of death among men cancer patients (the first is lung cancer), with a rate of 27,000 deaths every year. However, the triggering genes for prostate cancer formation are still ill-defined. Recently, SIRT1, a member of the sirtuin family, a group of sodium-dependent histone deacytylases, was suggested to either potentiate or repress the proliferation of cancer-cells in a cell-type specific manner. In this study, the authors generated a mouse model that lacks SIRT1 and discovered that these mice were more prone to develop prostatic intraepithelial neoplasia (PIN), i.e., a condition characterized by an abnormal morphology of prostate epithelial cells under the microscope and defined as an early form of prostate cancer. The researcher team showed that the lack of SIRT1 in this mouse model triggered the accumulation of intracellular reactive oxygen species (ROS), du
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