BCA3 contributes to the malignant progression of hepatocellular carcinoma through AKT activation and NF-κB translocation
Journal Article
·
· Experimental Cell Research
- Department of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe East Road, Zhengzhou, Henan (China)
- Henan Key Laboratory of Digestive Organ Transplantation (China)
Highlights: • The expression of BCA3 was up-regulated in HCC. • Up-regulation of BCA3 promoted proliferation, migration, invasion of HCC cells and tubular formation of HUVECs. • BCA3 promoted AKT activation and NF-κB translocation. Hepatocellular carcinoma (HCC) is one of the most lethal malignancies worldwide with elusive molecular mechanisms. The aim of this study is to investigate the clinical significance and biological roles of breast cancer-associated protein 3 (BCA3) in HCC. Our investigation demonstrated that BCA3 expression was up-regulated in primary HCC tissues, and BCA3 levels were positively correlated with tumor size, TNM stage, microvascular invasion and poor prognosis. BCA3 promoted tumor growth, metastasis and angiogenesis of HCC in vitro and in vivo. Moreover, we found that BCA3 induced aggressive behaviors were mediated by AKT activation, which in turn activated mTOR signalling pathway and induced cytoplasm-nuclear translocation of NF-κB p65. Blockage of AKT signalling pathway by a specific AKT inhibitor LY294002 impaired BCA3 mediated phenotypes. Collectively, our current study indicated the pleiotropic effects of BCA3 in HCC progression, and blockage of BCA3-AKT pathway might contribute to development of therapeutic measures for HCC.
- OSTI ID:
- 23082537
- Journal Information:
- Experimental Cell Research, Journal Name: Experimental Cell Research Journal Issue: 1 Vol. 362; ISSN 0014-4827; ISSN ECREAL
- Country of Publication:
- United States
- Language:
- English
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