Vitamin D regulates cell viability, migration and proliferation by suppressing galectin-3 (Gal-3) gene in ovarian cancer cells

ABSTRACT

Vitamin D deficiency is identified as a risk factor for the occurrence and recurrence of ovarian cancer.Galectin-3 (Gal-3) participates in many physiological and pathological processes. In present study, serumvitamin D level was detected using chemiluminescence enzyme immunoassay. Gal-3 expression wasexamined using real-time polymerase chain reaction (PCR), Western blot and immunocytochemistry analysis. SKOV3 cells viability was assessed by the water-soluble tetrazolium salt (WST-1) assay, the migrationof SKOV3 cells was detected using transwell assay, and the proliferation of SKOV3 cells was measured by3H-thymidine incorporation (3H-TdR). Our study demonstrated that vitamin D levels were lower in 40ovarian cancer patients vitamin D deficiency is closely related to the pathogenesis of ovarian cancer.Treatment with vitamin D reduced the migration and proliferation of ovarian cancer cells. Gal-3 wasoverexpressed in ovarian cancer, which could induce the viability, migration and proliferation ability ofovarian cancer cells, and these effects were abrogated by vitamin D downregulating the expression of Gal-3gene. Therefore, our results support that vitamin D may suppress Gal-3-induced viability, migration andproliferation ability of ovarian cancer cells, which suggests that the use of vitamin D may have beneficialeffects in preventing and treating ovarian cancer.