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YSY01A, a Novel Proteasome Inhibitor, Induces Cell Cycle Arrest on G2 Phase in MCF-7 Cells via ER alpha and PI3K/Akt Pathways
Xue, Bingjie1; Huang, Wei1; Yuan, Xia1; Xu, Bo2; Lou, Yaxin3; Zhou, Quan1; Ran, Fuxiang1; Ge, Zemei4; Li, Runtao4; Cui, Jingrong1
关键词YSY01A PS341 MCF-7 High-content screening Label-free quantitative proteomics ER alpha PI3K/Akt pathways
刊名JOURNAL OF CANCER
2015
DOI10.7150/jca.10733
6期:4页:319-326
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology
资助者Ministry of National Science and Technology National Major Scientific and Technological Special Project for "Significant New Drugs Development" Program ; State Key Program of National Natural Science Foundation of China ; Ministry of National Science and Technology National Major Scientific and Technological Special Project for "Significant New Drugs Development" Program ; State Key Program of National Natural Science Foundation of China
研究领域[WOS]Oncology
关键词[WOS]BORTEZOMIB-INDUCED APOPTOSIS ; METASTATIC BREAST-CANCER ; ESTROGEN-RECEPTOR-ALPHA ; MULTIPLE-MYELOMA ; THERAPEUTIC TARGET ; GROWTH ; TRANSCRIPTION ; CARFILZOMIB ; RESISTANCE ; REGULATORS
英文摘要

Given that the proteasome is essential for multiple cellular processes by degrading diverse regulatory proteins, inhibition of the proteasome has emerged as an attractive target for anti-cancer therapy. YSY01A is a novel small molecule compound targeting the proteasome. The compound was found to suppress viability of MCF-7 cells and cause limited cell membrane damage as determined by sulforhodamine B assay (SRB) and CytoTox 96 (R) non-radioactive cytotoxicity assay. High-content screening (HCS) further shows that YSY01A treatment induces cell cycle arrest on G2 phase within 24 hrs. Label-free quantitative proteomics (LFQP), which allows extensive comparison of cellular responses following YSY01A treatment, suggests that various regulatory proteins including cell cycle associated proteins and PI3K/Akt pathway may be affected. Furthermore, YSY01A increases p-CDC-2, p-FOXO3a, p53, p21(Cip1) and p27(Kip1) but decreases p-Akt, p-ER alpha as confirmed by Western blotting. Therefore, YSY01A represents a potential therapeutic for breast cancer MCF-7 by inducing G2 phase arrest via ER alpha and PI3K/Akt pathways.

语种英语
所属项目编号2009 ZX0930010 ; 81172915
资助者Ministry of National Science and Technology National Major Scientific and Technological Special Project for "Significant New Drugs Development" Program ; State Key Program of National Natural Science Foundation of China ; Ministry of National Science and Technology National Major Scientific and Technological Special Project for "Significant New Drugs Development" Program ; State Key Program of National Natural Science Foundation of China
WOS记录号WOS:000353062600003
引用统计
被引频次:4[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/64091
专题北京大学药学院
作者单位1.Peking Univ, Sch Pharmaceut Sci, State Key Lab Nat & Biomimet Drugs, Beijing 100083, Peoples R China
2.Peking Univ, Sch Pharmaceut Sci, Instrumental Anal Ctr, State Key Lab Nat & Biomimet Drugs, Beijing 100083, Peoples R China
3.Peking Univ, Lab Prote Med & Hlth Analyt Ctr, Beijing 100083, Peoples R China
4.Peking Univ, Sch Pharmaceut Sci, Dept Med Chem, Beijing 100083, Peoples R China
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GB/T 7714
Xue, Bingjie,Huang, Wei,Yuan, Xia,et al. YSY01A, a Novel Proteasome Inhibitor, Induces Cell Cycle Arrest on G2 Phase in MCF-7 Cells via ER alpha and PI3K/Akt Pathways[J]. JOURNAL OF CANCER,2015,6(4):319-326.
APA Xue, Bingjie.,Huang, Wei.,Yuan, Xia.,Xu, Bo.,Lou, Yaxin.,...&Cui, Jingrong.(2015).YSY01A, a Novel Proteasome Inhibitor, Induces Cell Cycle Arrest on G2 Phase in MCF-7 Cells via ER alpha and PI3K/Akt Pathways.JOURNAL OF CANCER,6(4),319-326.
MLA Xue, Bingjie,et al."YSY01A, a Novel Proteasome Inhibitor, Induces Cell Cycle Arrest on G2 Phase in MCF-7 Cells via ER alpha and PI3K/Akt Pathways".JOURNAL OF CANCER 6.4(2015):319-326.
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