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Mol Oncol. 2018 Dec;12(12):2042-2054. doi: 10.1002/1878-0261.12358. Epub 2018 Oct 26.

Nogo-B promotes tumor angiogenesis and provides a potential therapeutic target in hepatocellular carcinoma.

Author information

1
State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai, China.
2
Department of Liver Surgery, Liver Cancer Institute, Zhongshan Hospital, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Fudan University, Shanghai, China.

Abstract

Tumor angiogenesis is one of the hallmarks of cancer as well as an attractive target for cancer therapy. Characterization of novel pathways that act in parallel with the VEGF/VEGFR axis to promote tumor angiogenesis may provide insights into novel anti-angiogenic therapeutic targets. We found that the expression level of Nogo-B is positively correlated with tumor vessel density in hepatocellular carcinoma (HCC). While Nogo-B depletion inhibited tumor angiogenesis, Nogo-B overexpression promoted tumor angiogenesis in a tumor xenograft subcutaneous model of the human HCC cell line. Mechanically, Nogo-B regulates tumor angiogenesis based on its association with integrin αv β3 and activation of focal adhesion kinase. Moreover, Nogo-B antibody successfully abolished the function of Nogo-B in tumor angiogenesis in vitro and in vivo. Collectively, our results strongly suggest that Nogo-B is an important tumor angiogenic factor and blocking Nogo-B selectively inhibits tumor angiogenesis.

KEYWORDS:

Nogo-B; blocking antibody; hepatocellular carcinoma; integrin; tumor angiogenesis

PMID:
30019429
PMCID:
PMC6275258
DOI:
10.1002/1878-0261.12358
[Indexed for MEDLINE]
Free PMC Article

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