| 1 | Artemisinin derivatives inhibit epithelial ovarian cancer cells via autophagy-mediated cell cycle arrest显示文摘Epithelial ovarian cancer (EOC)is the most fatal gynecologic malignancy due to its late diagnosis and lack of curative therapy.The antimalaria compound artemisinin and its derivatives,such as artesunate (ART)and dihydroartemisinin (DHA),have proven to be potent anticancer drugs and act through various anticancer mechanisms.To identify novel targets of artemisinin derivatives in EOC cells,we investigated the effects of ART and DHA on SKOV3 and primary EOC cell growth via CCK-8 assay.Both ART and DHA inhibited EOC cell growth.A cell cycle distribution analysis showed that ART and DHA caused G2/M cell cycle arrest.Moreover,ART and DHA induced autophagy in EOC cells,whereas autophagy inhibitors reversed the cell growth inhibition and cell cycle arrest induced by ART and DHA.Western blot analysis showed that ART and DHA also suppressed the cell cycle-related NF-κB-signaling pathway in EOC cells.These data suggest that artemisinin derivatives induce autophagy,block the cell cycle,and inhibit cell growth in EOC cells.Our research provides new targets for artemisinin derivatives for EOC treatment. | Boning Li Shixia Bu Junyan Sun Ying Guo Dongmei Lai | 2018 | Acta Biochimica et Biophysica Sinica2018，50，12： | 11 |
| 2 | Low-dose cisplatin-induced CXCR4 expression promotes proliferation of ovarian cancer stem-like cells显示文摘Chemoresistance 堵住上皮的卵巢的癌症的有效治疗,它所有妇产科的癌症是最致命的。癌症干细胞被相信是至少为 chemoresistance 的发展部分负责。在这研究,癌症的丰富和增长上的 cisplatin (CDP ) 的效果像茎的房间(CSLC ) 被调查,并且行动的内在的机制被阐明。一在里面 vitro 没有锚的系统被采用从 SKOV3 人的上皮的卵巢的癌症房间线充实 CSLC。我们的结果证明有 CDP 的低集中的治疗导致了更好充实的 CSLC,与更高的 proliferative 活动。CDP 的低剂量被发现导致 chemokine (C-X-C 主题) 的表示受体 4 (CXCR4 ) ,它为卵巢的癌症治疗是在癌症干细胞以及一个有希望的治疗学的目标的一个重要 stemness 标记。结果也证明 overexpressed CXCR4 产生了 chemoresistance。把结果基于这些,在低集中, CDP 本身贡献药抵抗的发展,这可以被结束。这发现提供新奇卓见进位于 chemoresistance 下面的机制并且为上皮的卵巢的癌症治疗有重要治疗学的含意。 | Yifei Chen Shuying Wang Shixia Bu Minhua Xu Dongmei Lai | 2016 | Acta Biochimica et Biophysica Sinica2016，48，3： | 2 |
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