ArticleMolecular and cellular biochemistry2012
Overexpression of hepatitis B x-interacting protein in HepG2 cells enhances tumor-induced angiogenesis.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The trial behind it
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- HBXIP Regulates Gastric Cancer Glucose Metabolism and Malignancy Through PI3K/AKT and p53 Signaling.OncoTargets and therapy · 2020Article
- Oncoprotein LAMTOR5 Activates GLUT1 Via Upregulating NF-κB in Liver Cancer.Open medicine (Warsaw, Poland) · 2019Article
- Increased Expression of LAMTOR5 Predicts Poor Prognosis and Is Associated with Lymph Node Metastasis of Head and Neck Squamous Cell Carcinoma.International journal of medical sciences · 2019Article
- Oncogenic HBXIP enhances ZEB1 through Sp1 to accelerate breast cancer growth.Thoracic cancer · 2018Article
- The Interaction of lncRNA-HEIH and lncRNA-HULC with HBXIP in Hepatitis B Patients.Gastroenterology research and practice · 2018Article
- HBXIP overexpression is correlated with the clinical features and survival outcome of ovarian cancer.Journal of ovarian research · 2017Article
- HBXIP, a binding protein of HBx, regulates maintenance of the G2/M phase checkpoint induced by DNA damage and enhances sensitivity to doxorubicin-induced cytotoxicity.Cell cycle (Georgetown, Tex.) · 2017Article
- Upregulating the Expression of Survivin-HBXIP Complex Contributes to the Protective Role of IMM-H004 in Transient Global Cerebral Ischemia/Reperfusion.Molecular neurobiology · 2017Article
- Elevated HBXIP expression is associated with aggressive phenotype and poor prognosis in esophageal squamous cell carcinoma.American journal of cancer research · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is a common malignancy and a leading cause of cancer death worldwide. Hepatitis B x-interacting protein (HBXIP), a cofactor of survivin, was originally identified by binding with the C-terminus of the HBx and negatively regulated the activity of HBx. In this study, the effect of HBXIP on the hepatoma cells-induced angiogenesis was investigated. Proliferation and migration of human umbilical vein endothelial cells (HUVECs) were detected by MTT and transwell assay, respectively. Tube formation and chick chorioallantoic membrane model were used to observe the angiogenesis. Vascular endothelial growth factor activity was assayed using ELISA kits. Western blotting was performed to examine the protein expression. Our results indicated that overexpression of HBXIP increased HepG2 cell-induced endothelial cells migration, proliferation, and angiogenesis, which may be related to increasing phosphorylation of endothelial NO synthase in HUVECs. These results suggest that HBXIP may play an important role in tumorigenesis by enhancing angiogenesis in HCC.
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Registered trials
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