ArticleBMC cancer2008
Vav3 oncogene activates estrogen receptor and its overexpression may be involved in human breast cancer.
Article in BMC cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 74 citations in OpenAlex.
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- The scaffold RhoGAP protein ARHGAP8/BPGAP1 synchronizes Rac and Rho signaling to facilitate cell migration.Molecular biology of the cell · 2023Article
- Targeting HuR-Vav3 mRNA interaction prevents Pseudomonas aeruginosa adhesion to the cystic fibrosis airway epithelium.JCI insight · 2023Article
- The role of Vav3 expression for inflammation and cell death during experimental myocardial infarction.Clinics (Sao Paulo, Brazil) · 2023Article
- Vav Proteins in Development of the Brain: A Potential Relationship to the Pathogenesis of Congenital Zika Syndrome?Viruses · 2022Review
- LncRNA RP11-138J23.1 Contributes to Gastric Cancer Progression by Interacting With RNA-Binding Protein HuR.Frontiers in oncology · 2022Article
- Differential gene expression in liver of colored broiler chicken divergently selected for residual feed intake.Tropical animal health and production · 2021Article
- The guanine nucleotide exchange factor VAV3 participates in ERBB4-mediated cancer cell migration.The Journal of biological chemistry · 2020Article
- QuaDMutNetEx: a method for detecting cancer driver genes with low mutation frequency.BMC bioinformatics · 2020Article
- Characterization of FGD5 Expression in Primary Breast Cancers and Lymph Node Metastases.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2018Article
- Evaluation of Vav3.1 as prognostic marker in endometrial cancer.Journal of cancer research and clinical oncology · 2018Article
- Widespread alternative exon usage in clinically distinct subtypes of Invasive Ductal Carcinoma.Scientific reports · 2017Article
- Therapeutic sensitivity to Rac GTPase inhibition requires consequential suppression of mTORC1, AKT, and MEK signaling in breast cancer.Oncotarget · 2017Article
- Inhibition of Vav3 gene can promote apoptosis of human gastric cancer cell line MGC803 by regulating ERK pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundOur previous study revealed that Vav3 oncogene is overexpressed in human prostate cancer, activates androgen receptor, and stimulates growth in prostate cancer cells. The current study is to determine a potential role of Vav3 oncogene in human breast cancer and impact on estrogen receptor a (ERalpha)-mediated signaling axis.
methodsImmunohistochemistry analysis was performed in 43 breast cancer specimens and western blot analysis was used for human breast cancer cell lines to determine the expression level of Vav3 protein. The impact of Vav3 on breast cancer cell growth was determined by siRNA knockdown of Vav3 expression. The role of Vav3 in ERalpha activation was examined in luciferase reporter assays. Deletion mutation analysis of Vav3 protein was performed to localize the functional domain involved in ERalpha activation. Finally, the interaction of Vav3 and ERalpha was assessed by GST pull-down analysis.
resultsWe found that Vav3 was overexpressed in 81% of human breast cancer specimens, particularly in poorly differentiated lesions. Vav3 activated ERalpha partially via PI3K-Akt signaling and stimulated growth of breast cancer cells. Vav3 also potentiated EGF activity for cell growth and ERalpha activation in breast cancer cells. More interestingly, we found that Vav3 complexed with ERalpha. Consistent with its function for AR, the DH domain of Vav3 was essential for ERalpha activation.
conclusionVav3 oncogene is overexpressed in human breast cancer. Vav3 complexes with ERalpha and enhances ERalpha activity. These findings suggest that Vav3 overexpression may aberrantly enhance ERalpha-mediated signaling axis and play a role in breast cancer development and/or progression.
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