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SLXM-2, a derivative of cyclophosphamide: mechanism of growth inhibition on hepatocarcinoma 22 cells
Pang, Li-ping1; Huang, Wei2; Sun, Qi3; Guo, Wei1; Li, Run-tao3; Cui, Jing-rong1,2
关键词cell cycle arrest cyclophosphamide derivative hepatocarcinoma H-22 lethal dose 50 leukocytotoxic effect
刊名ANTI-CANCER DRUGS
2008-02-01
19期:2页:167-174
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]FISSION YEAST ; BREAST-CANCER ; DNA-DAMAGE ; NUCLEAR ; KINASE ; CYCLE ; PHOSPHORYLATION ; MITOSIS ; ACTIVATION ; THERAPY
英文摘要

Restructuring of cyclophosphamide (CPA) is a promising method for the development of antineoplastic therapy. This study investigated the inhibitory effects of a derivative of CPA, SLXM-2, on hepatocarcinoma 22 (H-22) transplanted into ICR mice as well as its effects on the survival time of mice transplanted with the ascitic fluid-type H-22. We found that SLXM-2 inhibited tumor growth and prolonged survival time. Moreover, the compound had little effect in vivo on leukocytes and body weight and a higher lethal dose 50 than CPA. The cell cycle analysis by flow cytometry revealed that SLXM-2 arrested tumor cells in both the S and G(2) phases, and the arrest in the G(2) phase increased in a dose-dependent manner. Western blotting and reverse transcription-PCR experiments indicated that the observed G(2) arrest was associated with an increase of cyclin B1, whereas cell division cycle protein 2 (Cdc2) remained constant. The results, however, showed an accumulation of tyrosine 15 phosphorylated Cdc2 and a reduction of threonine 161 phosphorylated Cdc2. In addition, SLXM-2 led to a decrease in cyclin-dependent kinase 7 and Cdc25c kinase, which participated in inhibiting the G(2)/M transition. Our data identified two upstream targets leading to the inactivity of the cyclin B1/Cdc2 complex, which explained the arrest in the G(2)/M phase following SLXM-2 treatment. These results demonstrated the antitumor activity of SLXM-2 and its potential use as an antineoplastic drug.

语种英语
WOS记录号WOS:000252479900008
Citation statistics
Cited Times:5[WOS]   [WOS Record]     [Related Records in WOS]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/60010
Collection北京大学药学院
北京大学药学院_天然药物与仿生药物国家重点实验室
北京大学药学院_化学生物学系
北京大学药学院_分子与细胞药理学系
作者单位1.Peking Univ, Sch Pharmaceut Sci, Hlth Sci Ctr, Natl Key Lab Nat & Biomimet Drugs, Beijing 100083, Peoples R China
2.Peking Univ, Sch Pharmaceut Sci, Hlth Sci Ctr, Dept Mol & Cellular Pharmacol, Beijing 100083, Peoples R China
3.Peking Univ, Sch Pharmaceut Sci, Hlth Sci Ctr, Dept Biol Chem, Beijing 100083, Peoples R China
Recommended Citation
GB/T 7714
Pang, Li-ping,Huang, Wei,Sun, Qi,et al. SLXM-2, a derivative of cyclophosphamide: mechanism of growth inhibition on hepatocarcinoma 22 cells[J]. ANTI-CANCER DRUGS,2008,19(2):167-174.
APA Pang, Li-ping,Huang, Wei,Sun, Qi,Guo, Wei,Li, Run-tao,&Cui, Jing-rong.(2008).SLXM-2, a derivative of cyclophosphamide: mechanism of growth inhibition on hepatocarcinoma 22 cells.ANTI-CANCER DRUGS,19(2),167-174.
MLA Pang, Li-ping,et al."SLXM-2, a derivative of cyclophosphamide: mechanism of growth inhibition on hepatocarcinoma 22 cells".ANTI-CANCER DRUGS 19.2(2008):167-174.
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