Although it’s widely accepted that inflammation is a critical underlying factor in a range of diseases, including the progression of cancer, little is known about its role when normal cells become tumor cells.
Now, scientists from the Florida campus of The Scripps Research Institute have shed new light on exactly how the activation of a pair of inflammatory signaling pathways leads to the transformation of normal breast cells to cancer cells.The study, led by Jun-Li Luo, an assistant professor at Scripps Florida, was published online before print by the journal Molecular Cell on February 23, 2012.
The researchers found immune/inflammatory cells ignite the transient activation of MEK/ERK and IKK/NF-kB pathways; the MEK/ERK pathway then directs a consistent activation of a signaling circuit in transformed cells. This consistent signaling circuit maintains the malignant state of the tumor cells.
Luo compares this process to starting a car—a car battery starts the engine much like the transient signal activation turns on the consistent signal circuit. Once the engine is started, it no longer needs the battery.
The scientists go on to show that the initial activation of these pathways also activates IL6, a cytokine involved in a number of inflammatory and autoimmune diseases, including cancer. IL6 acts as a tumor initiator, sparking the self-sustaining circuit in normal breast cells necessary for the initiation and maintenance of their transformed malignant state.
The first author of the study, “IL6-Mediated Suppression of Mir-200c Directs Constitutive Activation of an Inflammatory Signaling Circuit That Drives Transformation and Tumorigenesis,” is Matjaz Rokavec of Scripps Research. Other authors include Weilin Wu, also of Scripps Research.The study was supported by the National Institute of Health, the United States Department of Defense, the Florida Department of Health, and Frenchman’s Creek Women for Cancer Research.
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