ArticleOncoTargets and therapy2019
ZNF277 regulates ovarian cancer cell proliferation and invasion through inhibition of PTEN.
Article in OncoTargets and therapy, 2019. 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, 7 citations in OpenAlex.
- KIN17 modulates the WNT/β-catenin pathway and epithelial mesenchymal transition in non-small cell lung cancer.Scientific reports · 2025Article
- The dual role of RNA-binding proteins: promotion of tumorigenesis, drug resistance, and emerging therapeutic targets.Acta biochimica et biophysica Sinica · 2025Article
- Spatiotemporal single-cell architecture of gene expression in the Caenorhabditis elegans germ cells.Cell discovery · 2025Article
- Integrated multi-omics analysis of zinc-finger proteins uncovers roles in RNA regulation.Molecular cell · 2024Article
- Silencing PTEN in the fallopian tube promotes enrichment of cancer stem cell-like function through loss of PAX2.Cell death & disease · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
backgroundZNF277 is a transcription factor that is overexpressed in several cancers. However, its clinical role in ovarian cancer (OC) has not been reported yet. The present study aims to investigate the expression of ZNF277 in patients with OC, and to reveal the effects of ZNF277 on the proliferation, migration, and invasion of OC cells.
methodsUsing The Cancer Genome Atlas database, we found that higher expression of ZNF277 was correlated with poorer survival times of OC patients. This study used functional experiments, such as Cell Counting Kit-8 assay, colony formation assay, wound healing assay, and transwell invasion assay. Mechanistically, using quantitative chromatin immunoprecipitation assay, luciferase reporter assay, quantitative reverse-transcription PCR, and Western blot we identified the potential mechanism.
resultsWe confirmed for the first time that the expression of ZNF277 is significantly increased in OC tissues and cell lines and that it is closely associated with the adverse clinical features of OC patients. We demonstrated that overexpression of ZNF277 potentiated the proliferation, migration, and invasion of SKOV3 and OVCAR3 loss-of-function experiments showed that the silencing of ZNF277 reduced the proliferation, migration, and invasion of OC cells. Mechanistically, using quantitative chromatin immunoprecipitation assay, luciferase reporter assay, quantitative reverse-transcription PCR, and Western blot we identified that PTEN was a direct downstream target for ZNF277. PTEN expression antagonized the tumor-promoting function of ZNF277.
conclusionTaken together, the results of the current study demonstrated that ZNF277 exerted a promoting role in the progression of OC and might act as a promising biomarker and therapeutic target for OC patients.
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