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Polo-like Kinase 1: 타목시펜 저항성 유방암 치료의 신규 약물타겟 : Polo-like Kinase 1: a novel target for tamoxifen-resistant breast cancer therapy
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- Authors
- Advisor
- 강건욱
- Major
- 약학대학 약학과
- Issue Date
- 2015-02
- Publisher
- 서울대학교 대학원
- Keywords
- Tamoxifen-resistant breast cancer (TAMR-MCF-7) ; Polo-like kinase (Plk1) ; Epithelial-mesenchymal transition (EMT) ; E-cadherin ; N-cadherin ; Snail ; Vimentin ; Estrogen receptor (ER) ; BI (Boehringer Ingelheim)
- Description
- 학위논문 (석사)-- 서울대학교 대학원 : 약학과, 2015. 2. 강건욱.
- Abstract
- One of the most occurring cancers in women is breast cancer. Breast cancer is mostly diagnosed from women in post-menopause. Polo-like kinase 1 (Plk1), a serine/threonine protein kinase, is a regulator of completion of cell cycle. In our study, we used MCF-7 and Tamoxifen-resistant MCF-7 (TAMR-MCF-7) cell lines. Here we report that Plk1 overexpression mediates tamoxifen-resistance in MCF-7. BI 2536 is a dihydroteridinone derivative compound that inhibits the activity of Plk1 in an ATP-competitive manner. Our in vitro studies revealed that cell proliferation inhibition through BI 2536 was more sensitive in TAMR-MCF-7 cells than the parent MCF-7 cells. By performing TAMR-MCF-7 derived xenograft model, we identified BI 2536 inhibited tumor growth in vivo. Moreover, we observed that BI 2536 suppressed N-cadherin, Snail, Vimentin and recued loss of E-cadherin. These intriguing findings suggest Plk1 inhibition rescued epithelial-mesenchymal transition (EMT) in TAMR-MCF-7 cells. Our results propose that Plk1 represents a novel target for tamoxifen-resistant breast cancer therapy.
- Language
- English
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