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Crosstalk between NLRP12 and JNK during Hepatocellular Carcinoma

Department of Pathology, UT Southwestern Medical Center, Dallas, TX 75390, USA
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Int. J. Mol. Sci. 2020, 21(2), 496; https://doi.org/10.3390/ijms21020496
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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