| Summary: | 碩士 === 國立中興大學 === 生命科學系所 === 107 === Cancer has been the leading cause of death in Taiwan for many years, and breast cancer is the fourth leading cause of female cancer death. In many cancers, including breast cancer, enhancer of zeste homolog 2（EZH2） are overexpressed. EZH2 is an epigenetic regulatory protein that can catalyze trimethylation of histone H3 at lysine 27 （H3K27me3） in targeted gene, leading to silencing of EZH2-targeted gene expression. Previous studies have found that overexpression of EZH2 promotes epithelial-mesenchymal transition（EMT）, enhancing the ability of cancer cells to migration, invasion and drug resistance. Previously our laboratory demonstrated that EZH2 can be phosphorylated at threonine（Thr）487 by cyclin-dependent kinase 1（CDK1）, resulting in inhibiting EZH2 histone methyltransferase activity. If the Thr 487 of EZH2 was mutated to alanine（T487A -EZH2）, the T487A-EZH2 could promote the migratory and invasive abilities of cancer cells. Here, we investigated whether WT-EZH2 and T487A-EZH2 can affect the epithelial-mesenchymal transition and drug resistance of cancer cells. The results show that overexpression of WT-EZH2 and T487A-EZH2 could promote epithelial-mesenchymal transition, cell survival and drug resistance of breast cancer cells. In addition knockdown of WT-EZH2 and T487A-EZH2 using shRNAs inhibited epithelial-mesenchymal transition, cell survival and proliferation of breast cancer cells. However, the underlying regulatory mechanisms heed to be investigated further.
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