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Background   FOXD3  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  FOXD3  in OC.    Methods  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  FOXD3  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  FOXD3  on tumor growth was investigated through in vivo xenograft experiments.    Results  GEO data analysis showed that  FOXD3  was hypermethylated in OC tissues. Also, qRT-PCR revealed that  FOXD3  was low expressed and methylation-specific PCR (MSP) confirmed that the methylation level of  FOXD3  was hypermethylated. Combined treatment of 5-aza-2′-deoxycytidine (5-Aza-dC) could synergistically restored  FOXD3  expression. Finally, in vitro and in vivo experiments showed that demethylated  FOXD3  decreased cell proliferation and migration abilities, and increased the cell apoptosis. In vivo experiment detected that demethylated  FOXD3  restrained tumor growth.    Conclusions   FOXD3  could act as a tumor suppressor to inhibit cell proliferation, migration and promote cell apoptosis in OC cells.    Electronic supplementary material  The online version of this article (10.1186/s12935-019-0755-8) contains supplementary material, which is available to authorized users.

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