Rapamycin: Killing two birds with one stone

Rapamycin: Killing two birds with one stone

Inhibition of TOR signaling leads to extended longevity in both invertebrate and invertebrate species by modulating a number of downstream molecular pathways [1,2]. Drugs that inhibit the TOR pathway can serve as powerful tools to translate the effects of the TOR pathway on lifespan in simpler invertebrate model systems to more complex systems like mammals. One of the most promising drugs to slow aging is rapamycin, an inhibitor of TOR, which was previously shown to extend lifespan in mice when administered late in life [3]. As aging is one of the biggest risk factors for cancer, one of the outstanding questions is whether drugs that slow aging will also slow age-related increases in cancer incidence. A recent study describes how treatment of mice initiated early in life can not only retard aging but also slow age-related increase in cancer. Work by Anisimov and colleagues examines the impact on health and lifespan of Rapamycin treated inbred female mice from 2 months of age as compared to control littermates. However, its effects on aging if administered early and intermittently have not been known. Some of the effects include a significant decline in weight gain across the lifespan, a significant increase in regularity of estrous cycle before the onset of old age and more than 20% increase in survival rate along with increase of 10% in median lifespan. Rapamycin targets TOR, a Ser/Thr kinase, the kingpin of a conserved nutrient sensing pathway and causes decline in S6 Kinase (S6K) phosphorylation at nano-molar concentrations (3). It has been earlier reported in an S6k1-/- mouse there is an increase in life span by activation of AMPK and increased resistance against many age related diseases but no effect on age-related increase in cancer incidence [4]. Hence, this study suggests that Rapamycin might have protective effects on age-related cancers through downstream effectors of TOR other than S6K.  

oncoscience impact factor Zoya Demidenko Dr. Zoya N. Demidenko Zoya N. Demidenko , Ph.D. is Executive Manager of the Oncotarget journal . Oncotarget publishes high-impact research papers of general interest and outstanding significance and novelty in all areas of biology and medicine: in translational, basic and clinical research including but not limited to cancer research, oncogenes, oncoproteins and tumor suppressors, signaling pathways as potential targets for therapeutic intervention, shared targets in different diseases (cancer, benign tumors, atherosclerosis, eukaryotic infections, metabolic syndrome and other age-related diseases), chemotherapy, and new therapeutic strategies. After earning her Ph.D. in molecular biology, Zoya was awarded a Fogarty post-doctoral Fellowship from the National Institutes of Health in Bethesda, MD. After successful completion of post-doctoral training, she continued her professional career at George Washington University and Albert Einstein School of Medicine . In 2005 she cofounded the startup company Oncotarget Inc. which is focused on the development of anti-aging and anti-cancer drugs. Her research interests include signal transduction, cell cycle and cellular senescence, and their pharmacological targeting. In 2009 she cofounded the publishing house Impact Journals which specializes in publishing scientific journals. In 2011 she was selected to be a Member of the National Association of Professional Women .

Comments

Popular posts from this blog

Contact inhibition and high cell density deactivate the mammalian target of rapamycin pathway, thus suppressing the senescence program. Zoya N. Demidenko

Growth Stimulation Leads to Cellular Senescence When the Cell Cycle Is Blocked. Zoya N Demidenko

Accumulation of hypoxia-inducible factor-1 is limited by transcription-dependent depletion. Zoya N Demidenko