This discovery, published in the February 2009 issue of the Proceedings of the National Academy of Sciences (PNAS) and entitled, "Phosphorylation of p53 by IκB kinase 2 promotes its degradation by β-TrCP," provides fresh insight about how cells that have become inflamed due to exposure to high IKK2 activity, can become more susceptible to tumour development.
"Our recent discoveries have provided an explanation on the beneficial and harmful effects of inflammation that have baffled scientists for years," added Dr Tergaonkar. "While the natural inflammatory response serves to help the body clear infection, excessive inflammation, on the other hand, promotes cellular changes that lead to the uncontrolled growth of cells that characterizes cancer and enables its spread. These new insights involving NFκB, WIP1 and IKK2 are fostering new anti-inflammatory therapeutic approaches to human ailments ranging from inflammation (like sepsis) to cancer."
Shen Han-Ming, Ph.D., an expert in cancer cell biology at the National University of Singapore's Yong Loo Lin School of Medicine, said, "Taken together, the work in Dr Tergaonkar's lab has significantly advanced our understanding of the regulatory mechanisms of NFκB and expanded the functional scope of NFκB. More important, such findings offer new opportunities for modulation of the NFκB signaling pathway and for exploring new therapeutic strategies in various human diseases such as cancer and sepsis."
|Contact: Cathy Yarbrough|
Agency for Science, Technology and Research (A*STAR), Singapore