Faculty Collaboration Database

The Nogo-B receptor promotes human hepatocellular carcinoma cell growth via the Akt signal pathway. J Cell Biochem 2018 Sep;119(9):7738-7746

Date

06/16/2018

Pubmed ID

29904947

Pubmed Central ID

PMC7328129

DOI

10.1002/jcb.27125

Scopus ID

2-s2.0-85053497684 (requires institutional sign-in at Scopus site)   6 Citations

Abstract

Nogo-B receptor (NgBR) is a type I receptor with a single transmembrane domain and specifically binds to ligand Nogo-B. A previous study demonstrated that NgBR was highly expressed in human breast invasive ductal carcinoma and promoted epithelial-mesenchymal transition in breast tumor cells. Our recent work found that NgBR expression was associated with a poor prognosis in human patients with hepatocellular carcinoma (HCC). Here, we elucidate that the increased expression of NgBR contributes toward the increased cell growth of human HCC cells both in vitro and in vivo. Cell viability and clonogenic survival analysis results demonstrated that knockdown of NgBR inhibits the cell growth in human HCC cells, which correlates with a reduction in the phosphorylation of Akt levels. Furthermore, overexpression of NgBR by the cotransfected pIRES-NgBR plasmid together with NgBR siRNA in human HCC cells can rescue impaired phosphorylation of Akt levels in NgBR knockdown human HCC cells. In addition, cell viability analyses showed that NgBR overexpression can rescue the cell growth inhibition presented in human HCC NgBR knockdown cells. Taken together, our results suggest that NgBR potentially acts as an oncogene in HCC by increasing Akt activity. Thus, NgBR may represent a new potential diagnostic and therapeutic target for the treatment of HCC.

Author List

Dong C, Liu Y, Jiang K, Wang H, Qu W, Zhang C, Liang R, Gao Z, Zhao B, Miao Q, Shao S, Wang L

MESH terms used to index this publication - Major topics in bold

Animals
Carcinoma, Hepatocellular
Cell Line, Tumor
Cell Proliferation
Gene Knockdown Techniques
Hep G2 Cells
Humans
Liver Neoplasms
Male
Mice
Neoplasm Transplantation
Phosphorylation
Proto-Oncogene Proteins c-akt
Receptors, Cell Surface
Signal Transduction