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NLRC5 promotes cell proliferation via regulating the AKT/VEGF-A signaling pathway in hepatocellular carcinoma.

Authors: He, Ying-Hua  Li, Ming-Fang  Zhang, Xing-Yan  Meng, Xiao-Ming  Huang, Cheng  Li, Jun 
Citation: He YH, etal., Toxicology. 2016 Jun 1;359-360:47-57. doi: 10.1016/j.tox.2016.06.012. Epub 2016 Jun 23.
Pubmed: (View Article at PubMed) PMID:27338800
DOI: Full-text: DOI:10.1016/j.tox.2016.06.012

NLRC5, a newly found member of the NLR family and the largest member of nucleotide-binding, has been reported to regulate immune responses and is associated with hepatocellular carcinoma (HCC). We investigated the mechanisms and signaling pathways of NLRC5 in HCC progression. Increased expression of NLRC5, vascular endothelial growth factor-A (VEGF-A) were found in human HCC tissue. There was a positive correlation between NLRC5 and VEGF-A expression and cell proliferation were enhanced in NLRC5-overexpressing HepG2 cells, but inhibited in cells with NLRC5 silencing treatment. Interestingly, we found that up-regulation of NLRC5 also coordinated the activation of PI3K/AKT signaling pathway. An AKT inhibitor LY294002 blocked VEGF-A expression and AKT phosphorylation in HepG2 cells and NLRC5-overexpressing HepG2 cells. These results demonstrate that NLRC5 promotes HCC progression via the AKT/VEGF-A signaling pathway.


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CRRD Object Information
CRRD ID: 15003194
Created: 2019-11-07
Species: All species
Last Modified: 2019-11-07
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.