Recent progress in genetics of aging, senescence and longevity: focusing on cancer-related genes
Metrics: PDF 2085 views | HTML 1862 views | ?
Albert E. Berman1, Olga V. Leontieva2, Venkatesh Natarajan2, James A. McCubrey3, Zoya N. Demidenko2, Mikhail A. Nikiforov2
1 V.N. Orekhovich Institute of Biomedical Chemistry RAMS, 10 Pogodinskaya Str., Moscow, Russia
2 Department Cell Stress Biology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY
3 Department of Microbiology & Immunology, Brody School of Medicine at East Carolina University, Greenville, NC
Albert E. Berman, email:
Keywords: senescence, quasi-programmed aging, diseases, cancer
Received: December 20, 2012, Accepted: December 30, 2012, Published: December 30, 2012
It is widely believed that aging results from the accumulation of molecular damage, including damage of DNA and mitochondria and accumulation of molecular garbage both inside and outside of the cell. Recently, this paradigm is being replaced by the “hyperfunction theory”, which postulates that aging is caused by activation of signal transduction pathways such as TOR (Target of Rapamycin). These pathways consist of different enzymes, mostly kinases, but also phosphatases, deacetylases, GTPases, and some other molecules that cause overactivation of normal cellular functions. Overactivation of these sensory signal transduction pathways can cause cellular senescence, age-related diseases, including cancer, and shorten life span. Here we review some of the numerous very recent publications on the role of signal transduction molecules in aging and age-related diseases. As was emphasized by the author of the “hyperfunction model”, many (or actually all) of them also play roles in cancer. So these “participants” in pro-aging signaling pathways are actually very well acquainted to cancer researchers. A cancer-related journal such as Oncotarget is the perfect place for publication of such experimental studies, reviews and perspectives, as it can bridge the gap between cancer and aging researchers.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.