| Summary: | 碩士 === 中國醫藥大學 === 癌症生物學研究所碩士班 === 101 === Breast cancer is one of the most common cancers in women in Taiwan. It has been ranked as the fourth leading cause of cancer death in Taiwan in 2012. Enhancer of zeste homolog 2 (EZH2) is a catalytic subunit of polycomb repressive complex 2 (PRC2), which trimethylates histone H3 on lysine 27, resulting in repressing gene transcription. It has been reported that EZH2 is overexpressed in many cancers including breast and prostate cancers, and epigenetically silences tumor suppressor genes that plays a pivotal role in cancer progression and metastasis. Previously we have demonstrated that EZH2 can be phosphorylated by cyclin-dependent kinase 1 (CDK1) at Thr487. The phosphorylation of EZH2 at Thr487 disrupts EZH2 binding with other PRC2 components SUZ12 and EED, and thereby inhibits its methyltransferase activity. In addition, breast cancer cells expressing mutant EZH2-T487A show higher migration and invasion ability compared with breast cancer cells expressing wild-type(WT) EZH2.However, the underlying mechanism is still unclear. In this study, we further explore the roles of phosphorylation of EZH2 at Thr487 in cancer cell migration and invasion.
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