Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2016) 41 EP582 | DOI: 10.1530/endoabs.41.EP582

ECE2016 Eposter Presentations Endocrine Disruptors (6 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

Geon-Tae Park , So-Ye Jeon & Kyung-Chul Choi


Laboratory of Biochemistry and Immunology, College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea.


Cigarette smoke contains over 60 well established carcinogens. There are strong links between some of these carcinogens and various types of smoking-induced cancers. In this study we investigated whether cigarette smoke extracts (CSEs) affects the cell proliferation, migration, and invasion of BG-1 human ovarian cancer cells by alteration of epithelial-mesenchymal transition (EMT). We confirmed that CSEs increased the ovarian cancer cell viability in a dose-dependent manner. Also the protein expression of cyclin D1 and cyclin E1 was increased while p21 and p27 expression was decreased by treatment of all CSEs (3R4F and two-domestic commercial cigarettes). Additionally the alteration of EMT markers such as E-cadherian and N-cadherin was examined. The expression of E-cadherin was reduced by the treatment of CSEs while its reverse transition marker N-cadherin was increased. EMT-associated transcriptional factors, Snail and Slug were also up-regulated by CSEs treatment. These results indicate that CSEs can increase EMT process in BG-1 ovarian cancer cells, which is associated with cancer cell migration. We examined the migration activity through scratch assay and fibronectin coated trans-well invasion assay, in which CSEs increased cancer cell migratory propensity. These functional alterations were associated with changes in the metastasis-related genes. Upon CSEs stimulation, the expression of MMP-9 and cathepsin D was increased. Taken together, we confirmed that CSEs increased the growth of human ovarian cancer cells and the development of metastasis by stimulating cell cycle and EMT process through up- and down-regulation of a multiple cellular markers and signaling proteins and that CSEs exposure might have a higher risk of ovarian cancer than nonsmokers. Based on the results of this in vitro study, we will examine the in vivo risk assessment of CSEs in a xenografted mouse model transplanted with BG-1 human ovarian cancer cells.

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