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ZNF277 regulates ovarian cancer cell proliferation and invasion through inhibition of PTEN

BACKGROUND: ZNF277 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 prolifera...

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Detalles Bibliográficos
Autores principales: Liu, Zhengling, Xu, Zonglan, Tian, Yonghui, Yan, Hua, Lou, Yanyan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6476229/
https://www.ncbi.nlm.nih.gov/pubmed/31114246
http://dx.doi.org/10.2147/OTT.S192553
Descripción
Sumario:BACKGROUND: ZNF277 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. METHODS: Using 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. RESULTS: We 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. CONCLUSION: Taken 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.