Gaillardin Suppresses Metastatic Progression of Human Ovarian Cancer through Modulation of Epithelial–Mesenchymal Transition and Angiogenesis-Related Factors

Ovarian cancer ranks as the seventh most prevalent malignancy and the fifth leading cause of mortality among females globally. Gaillardin, a sesquiterpene lactone compound, exhibits anticancer properties across various tumor cell types. The aim of this investigation was to evaluate the antiproliferative impact of gaillardin on the SKOV3 ovarian carcinoma cell line. Cell growth inhibition in SKOV3 cultures was determined via the MTT assay, with subsequent calculation of IC50 concentrations. The effects on cell migration and invasion post-gaillardin exposure were examined through scratch wound healing experiments. Quantitative real-time PCR was employed to assess transcript levels of key epithelial-mesenchymal transition (EMT) genes, including CDH1, CDH2, VIM, and FN1, as well as angiogenesis-related genes VEGFA and THBS1. Protein levels of E-cadherin, N-cadherin, vimentin, fibronectin 1, VEGFA, and thrombospondin 1 were analyzed by Western blot technique. Treatment with gaillardin markedly reduced SKOV3 cell viability relative to untreated groups. Additionally, exposed cells displayed reduced migration and invasive capabilities compared to controls. Gene expression analysis via real-time PCR indicated that gaillardin significantly enhanced CDH1 and THBS1 mRNA levels while suppressing CDH2, VIM, FN1, and VEGFA transcripts. Comparable patterns were observed in the protein expression profiles of these factors. These findings suggest that gaillardin could potentially inhibit tumor growth and metastatic spread in ovarian carcinoma cells. Its antimetastatic actions appear to target pathways involved in both EMT and angiogenesis.