Crosstalk between NLRP12 and JNK during Hepatocellular Carcinoma
Open Access
- 12 January 2020
- journal article
- review article
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 21 (2), 496
- https://doi.org/10.3390/ijms21020496
Abstract
Hepatocellular carcinoma (HCC), a leading cause of cancer-related death, is initiated and promoted by chronic inflammation. Inflammatory mediators are transcriptionally regulated by several inflammatory signaling pathways, including nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK). cJun N-terminal kinase (JNK), a member of the MAPK family, plays a central role in HCC pathogenesis. Pathogen-associated molecular patterns (PAMPs) activate JNK and other MAPK upon recognition by toll-like receptors (TLRs). Apart from TLRs, PAMPs are sensed by several other pattern recognition receptors, including cytosolic NOD-like receptors (NLRs). In a recent study, we demonstrated that the NLR member NLRP12 plays a critical role in suppressing HCC via negative regulation of the JNK pathway. This article briefly reviews the crosstalk between NLRP12 and JNK that occurs during HCC.Funding Information
- Cancer Prevention and Research Institute of Texas (RP160169)
This publication has 94 references indexed in Scilit:
- NLRP12 Suppresses Colon Inflammation and Tumorigenesis through the Negative Regulation of Noncanonical NF-κB SignalingImmunity, 2012
- Promotion of Hepatocellular Carcinoma by the Intestinal Microbiota and TLR4Cancer Cell, 2012
- Inflammasomes and intestinal tumorigenesisDrug Discovery Today: Disease Mechanisms, 2012
- Clinical presentation and pathogenesis of cold-induced autoinflammatory disease in a family with recurrence of an NLRP12 mutationArthritis & Rheumatism, 2011
- NF-κB and STAT3 – key players in liver inflammation and cancerCell Research, 2010
- Pattern Recognition Receptors and InflammationCell, 2010
- Dietary and Genetic Obesity Promote Liver Inflammation and Tumorigenesis by Enhancing IL-6 and TNF ExpressionCell, 2010
- Hepatocyte Necrosis Induced by Oxidative Stress and IL-1α Release Mediate Carcinogen-Induced Compensatory Proliferation and Liver TumorigenesisCancer Cell, 2008
- p38α suppresses normal and cancer cell proliferation by antagonizing the JNK–c-Jun pathwayNature Genetics, 2007
- Inflammation and cancerNature, 2002