| Summary: | 碩士 === 國立中興大學 === 生命科學系所 === 106 === Ovarian cancer is one of the top ten causes of cancer death among women. Ovarian cancer has not obvious symptoms, which can result in late detection. Paclitaxel is used as first line therapy for advanced ovarian cancer. Roughly 70% of ovarian cancers are sensitive to chemotherapy at diagnosis, but rapidly develop drug resistance and metastasis leading to treatment failure and disease progression. Enhancer of zeste homolog 2 (EZH2) is a histone methyltransferase. EZH2 has been identified as a catalytic subunit of Polycomb Repressive Complex 2 (PRC2) for tri-methylation of histone H3 at Lys 27 (H3K27me3) by SET domain in its C-terminus. It silences targeted genes and mediates the activation of epithelial to mesenchymal transition (EMT) in many cancers. EZH2 is involved in various biological functions, such as cell proliferation, cell cycle and cell differentiation. To further investigate the expression and mechanism of EZH2 in ovarian cancer cells. We used western blotting to detect the expression of EZH2 in ovarian cancer cells. Transwell assays prove that EZH2 can promote the migration and invasion of ovarian cancer cells. Inhibition of EZH2 expression using shRNA can reduce the migration and invasion of ovarian cancer cells. To observe the effects of EZH2 on EMT of ovarian cancer cells by western blotting, the results show that EZH2 inhibits epithelial markers and promotes the expression of mesenchymal markers to cause EMT in ovarian cancer cells. Moreover, the effects of EZH2 on cell survival and paclitaxel resistance were evaluated by cell viability assay. Inhibition of EZH2 can reduce the drug resistance and cell viability of ovarian cancer cells
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