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Crosstalk between NLRP12 and JNK during Hepatocellular Carcinoma

Department of Pathology, UT Southwestern Medical Center, Dallas, TX 75390, USA
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(2), 496;
Received: 19 December 2019 / Revised: 31 December 2019 / Accepted: 8 January 2020 / Published: 13 January 2020
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. View Full-Text
Keywords: JNK; NLRP12; hepatocellular carcinoma; inflammation JNK; NLRP12; hepatocellular carcinoma; inflammation
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Khan, S.; Zaki, H. Crosstalk between NLRP12 and JNK during Hepatocellular Carcinoma. Int. J. Mol. Sci. 2020, 21, 496.

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