AICAR inhibits proliferation and induced S-phase arrest, and promotes apoptosis in CaSki cells

doi:10.1111/j.1745-7254.2007.00675.x

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	AICAR inhibits proliferation and induced S-phase arrest, and promotes apoptosis in CaSki cells
	Guan, TJ; Qin, FJ; Du, JH; Geng, L; Zhang, YY; Li, M; Zhang, YY (reprint author), Lanzhou Univ, Sch Bas Med, Inst Pathol, Lanzhou 730000, Peoples R China.
刊名	ACTA PHARMACOLOGICA SINICA
	2007-12
卷号	28 期号:12 页码:1984-1990
关键词	AICAR proliferation apoptosis CaSki cells
ISSN号	1671-4083
DOI	10.1111/j.1745-7254.2007.00675.x
文献子类	Article
英文摘要	Aim: The aim of the present study was to determine the effect of 5-aminoimidazole-4-carboxamide-ribonucleoside (AICAR) on proliferation, cell cycle, and apoptosis in the human epithelial cervical cancer cell line CaSki cells. Methods: Cell count and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay were used to determine cell proliferation and viability. Hoechst 33258 staining was conducted to distinguish the apoptotic cells. Cell cycle and Annexin-V/propidium iodide staining were analyzed by fluorescence-activated cell sorting (FACS). A Western blot assay was used to evaluate the expression of AKT (also known as protein kinase B), mammalian target of rapamycin (mTOR), p53, and extracellular signal-regulated kinase (ERK). Results: AICAR (500 mu mol/L) significantly inhibited the proliferation of CaSki cells treated for 24, 48, and 72 h as determined by cell count. The cells at the G(1) and G(2) phases were dramatically decreased while cells at the S phase were increased in response to AICAR treatment for 24, 48, and 72 h. The MTT assay showed less viable cells and Hoechst fluorescent staining showed more apoptotic cells upon AICAR stimulation. The results of the Annexin-V staining demonstrated a time-dependent increase of apoptosis in cells treated with AICAR for 24, 36, and 48 h. Furthermore, AICAR activated caspase-3 in a time-dependent manner. It was also found that AICAR inhibited the phosphory-lation of AKT and mTOR, which are important kinases regulating cell growth and survival. AICAR stimulation obviously increased the expression of the tumor suppressor p53 and the phosphorylation of ERK. Conclusion: AICAR inhibited proliferation and induced S phase arrest and promoted apoptosis in CaSki cells, which might be mediated by the downregulation of the AKT/mTOR pathway and the upregulation of the p53/ERK pathway.
学科主题	Chemistry ; Pharmacology & Pharmacy
出版地	OXFORD
语种	英语
CSCD记录号	CSCD:3089025
WOS记录号	WOS:000251327800016
内容类型	期刊论文
源URL	[http://ir.lzu.edu.cn/handle/262010/121376]
专题	基础医学院_期刊论文
通讯作者	Zhang, YY (reprint author), Lanzhou Univ, Sch Bas Med, Inst Pathol, Lanzhou 730000, Peoples R China.
推荐引用方式 GB/T 7714	Guan, TJ,Qin, FJ,Du, JH,et al. AICAR inhibits proliferation and induced S-phase arrest, and promotes apoptosis in CaSki cells[J]. ACTA PHARMACOLOGICA SINICA,2007,28(12):1984-1990.
APA	Guan, TJ.,Qin, FJ.,Du, JH.,Geng, L.,Zhang, YY.,...&Zhang, YY .(2007).AICAR inhibits proliferation and induced S-phase arrest, and promotes apoptosis in CaSki cells.ACTA PHARMACOLOGICA SINICA,28(12),1984-1990.
MLA	Guan, TJ,et al."AICAR inhibits proliferation and induced S-phase arrest, and promotes apoptosis in CaSki cells".ACTA PHARMACOLOGICA SINICA 28.12(2007):1984-1990.