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Geon-Tae Park DOI: 10.3252/pso.eu.18ECE.2016 Endocrine Disruptors In conclusion, CSEs increased proliferation and metastatic potential of BG-1 human ovarian cancer cells by stimulating the growth, migration and invasion of BG1 cells. In parallel, CSEs affected the expression of cell cycle related genes in a way to promote cell cycle transition as well as inhibited the expression of proapoptotic genes, leading to a decreased apoptosis. Also CSEs treatment promoted the EMT process through the upand downregulation of a multiple cellular markers and signaling proteins. These functional alterations were associated with changes in the metastasis-related genes such as MMP-9 and cathepsin D. Based on the results, CSEs exposure might have a higher risk of ovarian cancer than nonsmokers. Also it is hoped that this study provide new insights for the prevention and cure of CS induced cancer. ABSTRACT

endocrine abstracts

Epithelial-mesenchymal transition and estrogen receptor-dependent pathway are linked with ovarian cancer cell growth and migration caused by cigarette smoke extracts in human ovarian cancer cells