Cervical cancer is caused by persistent human papilloma virus types 16 and 18 infections. This cancer is classified as a malignancy due to its capability to invade and seed at distant sites to form metastases. Lymph nodes metastasis areis an important factor relating to cervical cancer survival. Our previous study reported eugenol from clove oil (Syzygium aromaticum) has anti-cancer effects by inducing apoptosis through p53 protein degradation inhibition in HeLa cancer cells. In this study, we continue to examine the anti-cancer eugenol effects as an anti-metastatic agent. A true experimental research with post-test only controlled group design was carried out on four groups of HeLa cell cultures receiving different eugenol concentrations. To identify the molecular mechanisms involved in the eugenol anti-metastatic effect, eugenol- treated HeLa cells were subjected to scratch wound healing and immunofluorescence staining assays. Both qualitative and quantitative approaches were carried out to analyze the obtained data. Quantitative methods such as one-way analysis of variance, Tukeys multiple comparison test, and Pearsons correlation were carried out. We show that eugenol effectively inhibits HeLa cell wound healing migration. Furthermore, we show the eugenol effect downregulated Snail-1 and vimentin protein expression and upregulated E-cadherin protein expression. These proteins are important regulators of epithelial-mesenchymal transition pathways.
Key words: Cervical cancer, E-cadherin, epithelial-mesenchymal transition, eugenol, HeLa cell,vimentin
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