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http://purl.uniprot.org/citations/19236751http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19236751http://www.w3.org/2000/01/rdf-schema#comment"This study was aimed to investigate the effects of arsenic trioxide (As(2)O(3)) and/or transforming growth factor-beta1 (TGF-beta1)on cell apoptosis and the changes of P27(Kip1), cyclin E and endogenous TGF-beta1 mRNA levels in NB4 cells. As(2)O(3) cytotoxicity to NB4 cells and the IC(50) were assayed with MTT, the apoptotic morphological changes were observed by Wright-Giemsa staining; the cell cycle and apoptosis were detected with flow cytometry. Semiquantitative RT-PCR was used to examine P27(Kip1), cyclin E and endogenous TGF-beta1 mRNA levels. The results showed that the As(2)O(3) and TGF-beta1 significantly suppressed the growth of NB4 cells, and promoted the apoptosis of these cells. The growth inhibition and apoptosis of NB4 cells treated with As(2)O(3) were in dose-and time-dependent manners. IC(50) were about 12 micromol/L for 24 hours, about 5 micromol/L for 48 hours, and about 3 micromol/L for 72 hours respectively. Cell cycle arrest in NB4 cells was induced by As(2)O(3) and/or TGF-beta1. The arrest of NB4 cells treated by 5 micromol/L As(2)O(3) was in G(2)/M phase, and 5 ng/ml TGF-beta1 in G(1) phase. However, the arrest of NB4 cells caused by combination of As(2)O(3) and TGF-beta1 was in S phase. After treating with As(2)O(3), P27(Kip1) and endogenous TGF-beta1 mRNA expressions of NB4 cells were up-regulated, and cyclin E mRNA expression was down-regulated. When NB4 cells were treated with TGF-beta1 alone, P27(Kip1) and cyclin E mRNA expressions were the same as that treated by As(2)O(3). Exogenous TGF-beta1 enhanced the above effects of As(2)O(3) in combination group. It is concluded that As(2)O(3) and TGF-beta1 are able to induce apoptosis and cell cycle abnormal distribution in NB4 cells. As(2)O(3) and exogenous TGF-beta1 may up-regulate endogenous TGF-beta1, which induce apoptosis of NB4 cells through consequently high expression of P27(Kip1). TGF-beta1 may lead to cell cycle arrest by inhibiting the expression of cyclin E directly, or by the activity of cyclin E through the increased expression of P27(Kip1)."xsd:string
http://purl.uniprot.org/citations/19236751http://purl.uniprot.org/core/author"Li Y."xsd:string
http://purl.uniprot.org/citations/19236751http://purl.uniprot.org/core/author"Liang Y."xsd:string
http://purl.uniprot.org/citations/19236751http://purl.uniprot.org/core/author"Li X."xsd:string
http://purl.uniprot.org/citations/19236751http://purl.uniprot.org/core/author"Wang Y."xsd:string
http://purl.uniprot.org/citations/19236751http://purl.uniprot.org/core/author"Wang P.P."xsd:string
http://purl.uniprot.org/citations/19236751http://purl.uniprot.org/core/author"Wang B.X."xsd:string
http://purl.uniprot.org/citations/19236751http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19236751http://purl.uniprot.org/core/name"Zhongguo Shi Yan Xue Ye Xue Za Zhi"xsd:string
http://purl.uniprot.org/citations/19236751http://purl.uniprot.org/core/pages"74-79"xsd:string
http://purl.uniprot.org/citations/19236751http://purl.uniprot.org/core/title"[P27(Kip1), cyclin E and endogenous TGF-beta1 changes in apoptosis of NB4 cells induced by As(2)O(3) and/or TGF-beta1 and their significance]."xsd:string
http://purl.uniprot.org/citations/19236751http://purl.uniprot.org/core/volume"17"xsd:string
http://purl.uniprot.org/citations/19236751http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/19236751
http://purl.uniprot.org/citations/19236751http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/19236751
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