FOXD3 may be a new cellular target biomarker as a hypermethylation gene in human ovarian cancer

is aberrantly regulated in several tumors, but its underlying mechanisms in ovarian cancer (OC) remains largely unknown. The present study aimed to explore the role and associated mechanisms of in OC. Microarray data from GEO was used to analyze differential CpG sites and differentially methylated regions (DMR) in tumor tissues and Illumina 450 genome-wide methylation data was employed. The expression level was determined through qRT-PCR and western blot analysis. Wound healing test, colony formation and flow cytometry assay were utilized to analyze cell migration, proliferation abilities, cell cycle and cell apoptosis, respectively. Finally, the effect of on tumor growth was investigated through in vivo xenograft experiments. GEO data analysis showed that was hypermethylated in OC tissues. Also, qRT-PCR revealed that was low expressed and methylation-specific PCR (MSP) confirmed that the methylation level of was hypermethylated. Combined treatment of 5-aza-2'-deoxycytidine (5-Aza-dC) could synergistically restored expression. Finally, in vitro and in vivo experiments showed that demethylated decreased cell proliferation and migration abilities, and increased the cell apoptosis. In vivo experiment detected that demethylated restrained tumor growth. could act as a tumor suppressor to inhibit cell proliferation, migration and promote cell apoptosis in OC cells.