The CCB seminar Wednesday 9th of March will be held by Geir Bjørkøy, professor at the Centre of Molecular Inflammation Research, Norwegian University of Science and Technology, Trondheim.
Title of his talk: Tumor-derived IL-6 contributes to cancer cachexia by increasing autophagy
Time and place: Mar 9, 2016 12:00 PM - 01:00 PM, Auditorium, New research building, Institute for Cancer Research, Montebello.
13:00 hrs: Refreshments and discussions in the lobby
The majority of cancer patients with advanced disease experience weight loss, including loss of lean body mass. Severe weight loss is a hallmark of cachexia, a condition that significantly impairs functional status and survival. The underlying causes of cachexia are incompletely understood and currently no therapeutic approach can completely reverse the condition. Elevated catabolism probably contributes to the syndrome. Autophagy is the major route for the degradation of cytosolic constituents and is systemically induced by starvation. We hypothesized that systemic acceleration of autophagy also occurs during cachexia, driven both by starvation-mimicking signaling compounds secreted from tumor cells and semi-starvation in patients. During our recent studies we have found evidence for an association between weight loss of the patient and autophagy-inducing bioactivity in the circulation. By using several cancer cell models for cachexia we identified IL-6 as an autophagy-inducing cytokine secreted from cancer cells. Recently, it has become evident that the in vivo activity of IL-6 is boosted by soluble IL-6 receptors and neutralized by association with soluble versions of the gp130 co-receptor. Thus, in cancer cachexia patients, autophagy may be regulated systemically via a complex network of proteins that regulates IL-6 bioactivity.
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