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学科主题: 基础医学
题名:
Inhibition of mouse embryonic carcinoma cell growth by lidamycin through down-regulation of embryonic stem cell-like genes Oct4, Sox2 and Myc
作者: Zhen, Hong-Ying1; He, Qi-Hua2; Zhen, Yong-Zhan3; Wang, Shu-Ling1; Liu, Yi-Nan1; Wu, Wei-Hua1; Zhang, Xiao-Yan1; Lu, Ai-Li1; Shen, Li1
关键词: Lidamycin ; Anti-cancer ; Mouse embryonic carcinoma (EC) cell ; Embryonic stem cell (ESC)-like genes-Oct4
刊名: INVESTIGATIONAL NEW DRUGS
发表日期: 2011-12-01
DOI: 10.1007/s10637-010-9463-x
卷: 29, 期:6, 页:1188-1197
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Oncology ; Pharmacology & Pharmacy
研究领域[WOS]: Oncology ; Pharmacology & Pharmacy
关键词[WOS]: TRANSCRIPTION FACTOR OCT4 ; RETINOIC ACID ; SOMATIC-CELLS ; SELF-RENEWAL ; CANCER-CELLS ; HUMAN TUMORS ; P19 CELLS ; DIFFERENTIATION ; EXPRESSION ; C-1027
英文摘要:

Lidamycin (LDM, also known as C-1027) as an anti-cancer agent inhibits growth in a variety of cancer cells by inducing apoptosis and cell cycle arrest. In this study we demonstrated that inhibition of mouse embryonic carcinoma (EC) cell growth using LDM at low concentrations can be attributed to a loss of the cell′s self-renewal capability but not to apoptosis or cell death, which can be correlated to the down-regulation of embryonic stem (ES) cell-like genes Oct4, Sox2 and c-Myc. MTT assays showed that LDM inhibited the growth of mouse P19 EC cells in a time- and dose-dependent manner. The EC cells exposed to a low dose (0.01 nM) of LDM lost their capability to generate colonies, as evidenced by the colony forming assay. Flow cytometer analyses demonstrated that LDM induced G1 arrest in exposed EC cells without apoptosis. Real-time qPCR, Western blotting and immunocytochemistry revealed that Oct4, Sox2 and c-Myc were down-regulated in LDM-exposed EC cells, but not adriamycin (ADM)-exposed cells. Furthermore, a combination of the low dose of LDM and ADM significantly reduced the proliferation of the cancer cells than single-agent treatment. This suggested that synergy of ADM and LDM improved chemotherapy. Taking together, our results indicate that LDM can reduce the capability for self-renewal that mouse EC cells possess through the repression of ES cell-like genes, thereby inhibiting carcinoma cell growth. This data also suggests that LDM might have potential for application in CSC-based therapy and be a useful tool for studying ES cell pluripotency and differentiation.

语种: 英语
项目资助者: Department of Cell Biology, Peking University Health Science Center ; Foundation of "211 Project" and "985 Project" in P R China
WOS记录号: WOS:000294824200007
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/63285
Appears in Collections:基础医学院_细胞生物学系_期刊论文

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作者单位: 1.Peking Univ, Dept Cell Biol, Hlth Sci Ctr, Beijing 100191, Peoples R China
2.Peking Univ, Med Anal Ctr, Hlth Sci Ctr, Beijing 100191, Peoples R China
3.N China Coal Med Univ, Dept Histol & Embryol, Tangshan 063000, Peoples R China

Recommended Citation:
Zhen, Hong-Ying,He, Qi-Hua,Zhen, Yong-Zhan,et al. Inhibition of mouse embryonic carcinoma cell growth by lidamycin through down-regulation of embryonic stem cell-like genes Oct4, Sox2 and Myc[J]. INVESTIGATIONAL NEW DRUGS,2011,29(6):1188-1197.
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