Abstract
IL-1 cytokines constitute a family of biologically active proteins with pleiotropic function especially in immunity. Both protective as well as deleterious properties of individual IL-1 family cytokines in tumor biology have been described. The function of IL-1-family cytokines depends on the producing source, the present (inflammatory) microenvironment and N-terminal proteolytical processing. Each of these determinants is shaped by different modes of cell death. Here we summarize the properties of IL-1 family cytokines in tumor biology, and how they are modulated by cell death.
Acknowledgments
We apologize to researchers whose primary observations could not be cited due to space limitations, which resulted in referring mainly to current reviews. Our work was supported by grants from Deutsche Forschungsgemeinschaft (SFB 1039 TP B06, Excellence Cluster Cardiopulmonary System), Deutsche Krebshilfe (110637), Else Kröner-Fresenius Foundation (EKFS) Research Training Groups Translational Research Innovation – Pharma (TRIP) and Else Kröner-Fresenius-Stiftung (Else Kröner-Fresenius-Graduate School, EKF-GK). J.M. was supported by Deutscher Akademischer Austauschdienst (DAAD) and the University of Costa Rica.
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©2016 Walter de Gruyter GmbH, Berlin/Boston
Articles in the same Issue
- Frontmatter
- Reviews
- Dynamic organization of the mitochondrial protein import machinery
- Common therapeutic strategies for prion and Alzheimer’s diseases
- IL-1 family cytokines in cancer immunity – a matter of life and death
- Research Articles/Short Communications
- Genes and Nucleic Acids
- Epigenetic regulation of KLK7 gene expression in pancreatic and cervical cancer cells
- Molecular Medicine
- Regulation of glycosylphosphatidylinositol-anchored proteins and GPI-phospholipase D in a c-Myc transgenic mouse model of hepatocellular carcinoma and human HCC
- Biological characteristics of renal cancer cells after CTP-mediated cancer suppressor gene NPRL2 protein treatment
- Cell Biology and Signaling
- Hepatitis B virus surface protein-induced hPIAS1 transcription requires TAL1, E47, MYOG, NFI, and MAPK signal pathways
- Inhibition of interleukin-3- and interferon- α-induced JAK/STAT signaling by the synthetic α-X-2′,3,4,4′-tetramethoxychalcones α-Br-TMC and α-CF3-TMC
- Vitamin C promotes pluripotency of human induced pluripotent stem cells via the histone demethylase JARID1A
Articles in the same Issue
- Frontmatter
- Reviews
- Dynamic organization of the mitochondrial protein import machinery
- Common therapeutic strategies for prion and Alzheimer’s diseases
- IL-1 family cytokines in cancer immunity – a matter of life and death
- Research Articles/Short Communications
- Genes and Nucleic Acids
- Epigenetic regulation of KLK7 gene expression in pancreatic and cervical cancer cells
- Molecular Medicine
- Regulation of glycosylphosphatidylinositol-anchored proteins and GPI-phospholipase D in a c-Myc transgenic mouse model of hepatocellular carcinoma and human HCC
- Biological characteristics of renal cancer cells after CTP-mediated cancer suppressor gene NPRL2 protein treatment
- Cell Biology and Signaling
- Hepatitis B virus surface protein-induced hPIAS1 transcription requires TAL1, E47, MYOG, NFI, and MAPK signal pathways
- Inhibition of interleukin-3- and interferon- α-induced JAK/STAT signaling by the synthetic α-X-2′,3,4,4′-tetramethoxychalcones α-Br-TMC and α-CF3-TMC
- Vitamin C promotes pluripotency of human induced pluripotent stem cells via the histone demethylase JARID1A