Article
Deregulation of the NLRP3 inflammasome in hepatic parenchymal cells during liver cancer progression

https://doi.org/10.1038/labinvest.2013.126Get rights and content
Under an Elsevier user license
open archive

Abstract

Hepatocellular carcinoma (HCC) is one of the most prevalent malignant tumors worldwide, and it is always the consequence of chronic hepatitis and liver cirrhosis. The nucleotide-binding domain, leucine-rich family (NLR), pyrin-containing 3 (NLRP3) inflammasome has been shown to orchestrate multiple innate and adaptive immune responses. However, little is known about its role in cancer. This study was performed to investigate the role of the NLRP3 inflammasome in the development and progression of HCC. The expression of NLRP3 inflammasome components was analyzed in HCC tissues and corresponding non-cancerous liver tissues at both the mRNA and protein levels. Our data demonstrate that the expression of all of the NLRP3 inflammasome components was either completely lost or significantly downregulated in human HCC, and that the deficiency correlated significantly with advanced stages and poor pathological differentiation. In addition, our data provide an overview of the expression of NLRP3 inflammasome components in the multi-stage development of HCC and indicate a surprising link between deregulation of the NLRP3 inflammasome molecular platform and HCC progression. In conclusion, this study presents a dynamic expression pattern of NLRP3 inflammasome components in multi-stage hepatocarcinogenesis and demonstrates that deregulated expression of the inflammasome is involved in HCC progression.

carcinogenesis
hepatocellular carcinoma
inflammasome
NLRP3
parenchymal cell

Cited by (0)

This study provides a comprehensive investigation of the multiprotein nucleotide-binding domain, leucine-rich family pyrin-containing-3 (NLRP3) inflammasome platform in the parenchymal cells of hepatocellular carcinoma (HCC) tissue. This study reveals a dynamic expression pattern of NLRP3 inflammasome components in the development of HCC and demonstrates that a deficiency of this molecular platform is involved in HCC progression.

5

Qing Wei and Kun Mu: These authors contributed equally to this work.