ArticleTranslational oncology2014
The Wilms' Tumor Gene WT1 - 17AA/- KTS Splice Variant Increases Tumorigenic Activity Through Up-Regulation of Vascular Endothelial Growth Factor in an In Vivo Ovarian Cancer Model.
Article in Translational oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Targeting the ST3 beta-galactoside alpha-2,3-sialyltransferase 1 (ST3Gal1) as a potential therapeutic strategy to overcome anti-VEGF resistance in endometrial cancer.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2025Article
- Alternative RNA splicing defects in pediatric cancers: new insights in tumorigenesis and potential therapeutic vulnerabilities.Annals of oncology : official journal of the European Society for Medical Oncology · 2022Review
- Transcription Factors in Cancer: When Alternative Splicing Determines Opposite Cell Fates.Cells · 2020Review
- Transcriptomic but not genomic variability confers phenotype of breast cancer stem cells.Cancer communications (London, England) · 2018Article
- Wilms' Tumor Protein 1 and Enzymatic Oxidation of 5-Methylcytosine in Brain Tumors: Potential Perspectives.Frontiers in cell and developmental biology · 2018Review
- Biomarker Expression Profiling in Cervix Carcinoma Biopsies Unravels WT1 as a Target of Artesunate.Cancer genomics & proteomicsArticle
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
The Wilms' tumor 1 gene WT1 encodes a zinc transcription factor involved in a variety of cancer-related processes. In this study, we sought to investigate the effects of WT1 splice variants on tumorigenic activity and survival in an in vivo ovarian cancer model. To this end, we established stable ovarian cancer cell lines transduced with lentiviral constructs containing each of the four WT1 splice variants (- 17AA/- KTS, + 17AA/- KTS, - 17AA/+ KTS, and + 17AA/+ KTS). In mice inoculated intraperitoneally with SKOV3ip1 cells expressing WT1 - 17AA/- KTS, disseminated tumor weights and production of ascites were significantly increased compared with those in mice inoculated with cells expressing the control vector. The overall survival in mice inoulated with WT1 - 17AA/- KTS-expressing cells was significantly shorter than that in mice inoculated with control cells (P = .0115). Immunoblot analysis revealed that WT1 - 17AA/- KTS significantly increased the expression of vascular endothelial growth factor (VEGF) compared with the control. Greater numbers of CD31-immunopositive vessels were observed in tumors from mice injected with cells expressing WT1 - 17AA/- KTS than in tumors from control mice. Finally, WT1 - 17AA/- KTS significantly increased tumor microvessel density compared with that in the control (P < .05). Treatment with anti-VEGF antibody (bevacizumab) inhibited tumor growth, dissemination, and ascites production in mice injected with cells expressing WT1 - 17AA/- KTS. The overexpression of WT1 - 17AA/- KTS induced a more aggressive phenotype in ovarian cancer cells through VEGF up-regulation in an in vivo ovarian cancer model. Our findings indicated that WT1 - 17AA/- KTS enhanced tumorigenic activity and could decreased patient survival through up-regulation of VEGF expression in ovarian cancers.
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Registered trials
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