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Molecular and Cellular Microbiology | Host-Microbe Interaction and Pathogenesis
Microbiol. Biotechnol. Lett.
Hyosun CHO 1, 2* and Wonhyeok CHOI 1, 2, 1
1Duksung women's university, 2Duksung Innovative Drug Center
Correspondence to :
Hyosun CHO, College of Pharmacy, Duksung Women’s University, Seoul, Republic of Korea [132-714]
Tel : 02-901-8678, Fax : 02-901-8386, E-mail : email@example.com
NLRP3 inflammasome plays an important role in the inflammatory responses through a recognition of pathogen-associated molecular patterns (PAMPs) and tumor progress including tumor growth as well as metastasis. In this study, we examined the effect of the defective NOD-like receptor pyrin domain-containing protein 3 (NLRP3) on hepatocellular carcinoma (HCC) SK-Hep1 tumor growth, migration and invasiveness. First, HCC SK-Hep1 was transfected with human NLRP3 targeting LentiCRISPRv2 vector using the CRISPR-Cas9 system and NLRP3 deficiency was confirmed by RT-qPCR and western blot. NLRP3 deficient SK-Hep1 showed a delayed cell growth along with decreased protein expressions of PI3K, p-AKT and pNF-κB compared to NLRP3 complete SK-Hep1. In addition, NLRP3 deficiency arrested cell cycle at G1 phase through increase of p21 and reduction of CDK6. NLRP3 deficient SK-Hep1 also presented significantly delayed characteristics in cell migration, invasion and wound healing. The expressions of epithelial-mesenchymal transition (EMT) signaling molecules such as N-cadherin and MMP-9 were found to be dramatically decreased in NLRP3 deficient SK-Hep1 compared to NLRP3 complete SK-Hep1.
Keywords: NLRP3, SK-Hep1, cell cycle, EMT