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NLRC5 regulates cell proliferation, migration and invasion in hepatocellular carcinoma by targeting the Wnt/β-catenin signaling pathway.

Abstract：

:NLRC5, the largest member of nucleotide-binding and oligomerization domain (NOD)-like receptor (NLR) family, has been reported to regulate immune responses and is associated with chronic inflammatory diseases. However, the biological function of NLRC5 in hepatocellular carcinoma (HCC) has not yet been well demonstrated. In this study, the role of NLRC5 in hepatocellular carcinoma cell proliferation, migration and invasion capacities was evaluated by using MTT, flow cytometry, wound healing, transwell assay, and tumor formation assay in nude mice. Western blot analysis and qPCR assay were performed to assess NLRC5 interacting with the activation of Wnt/β-catenin signaling pathway. Here, we demonstrate that NLRC5 was highly expressed in HCC. Knockdown of NLRC5 significantly inhibited cell proliferation, migration, invasion and the tumor formation in nude mice, and arrested the cell cycle at G0/G1 phase. Furthermore, overexpression of NLRC5 promoted the proliferation, migration and invasion of HCC cells in vitro. Interestingly, we found that up-regulation of NLRC5 not only positively correlates with the increase of β-catenin but also coordinates the activation of downstream Wnt/β-catenin signaling pathway. Thus, our findings suggest that NLRC5 may play an important role in progression of HCC and provide a potential therapeutic value in this tumor.

journal_name

Cancer Lett

journal_title

Cancer letters

authors

Peng YY,He YH,Chen C,Xu T,Li L,Ni MM,Meng XM,Huang C,Li J

doi

10.1016/j.canlet.2016.03.006

subject

Has Abstract

pub_date

2016-06-28 00:00:00

pages

10-21

issue

1

eissn

0304-3835

issn

1872-7980

pii

S0304-3835(16)30142-2

journal_volume

376

pub_type

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