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Inflammasomes in cancer: a double-edged sword |
Ryan Kolb1,Guang-Hui Liu2,3,Ann M. Janowski4,Fayyaz S. Sutterwala4,5,6,Weizhou Zhang1,*( ) |
1. Department of Pathology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA 2. National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China 3. Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA 4. Graduate Program in Immunology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA 5. Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA 6. Veterans Affairs Medical Center, Iowa City, IA 52241, USA |
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Abstract Chronic inflammatory responses have long been observed to be associated with various types of cancer and play decisive roles at different stages of cancer development. Inflammasomes, which are potent inducers of interleukin (IL)-1β and IL-18 during inflammation, are large protein complexes typically consisting of a Nod-like receptor (NLR), the adapter protein ASC, and Caspase-1. During malignant transformation or cancer therapy, the inflammasomes are postulated to become activated in response to danger signals arising from the tumors or from therapy-induced damage to the tumor or healthy tissue. The activation of inflammasomes plays diverse and sometimes contrasting roles in cancer promotion and therapy depending on the specific context. Here we summarize the role of different inflammasome complexes in cancer progression and therapy. Inflammasome components and pathways may provide novel targets to treat certain types of cancer; however, using such agents should be cautiously evaluated due to the complex roles that inflammasomes and proinflammatory cytokines play in immunity.
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inflammasome
cancer
inflammation
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Corresponding Author(s):
Weizhou Zhang
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Issue Date: 16 May 2014
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