[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].

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  • Author(s): Liang Y;Liang Y; Li Y; Wang Y; Li X; Wang PP; Wang BX
  • Source:
    Zhongguo shi yan xue ye xue za zhi [Zhongguo Shi Yan Xue Ye Xue Za Zhi] 2009 Feb; Vol. 17 (1), pp. 74-9.
  • Publication Type:
    Journal Article; Research Support, Non-U.S. Gov't
  • Language:
    Chinese
  • Additional Information
    • Source:
      Publisher: Zhongguo shi yan xue za zhi she Country of Publication: China NLM ID: 101084424 Publication Model: Print Cited Medium: Print ISSN: 1009-2137 (Print) Linking ISSN: 10092137 NLM ISO Abbreviation: Zhongguo Shi Yan Xue Ye Xue Za Zhi Subsets: MEDLINE
    • Publication Information:
      Original Publication: Beijing : Zhongguo shi yan xue za zhi she,
    • Subject Terms:
      Apoptosis/*drug effects ; Arsenicals/*pharmacology ; Cyclin E/*metabolism ; Cyclin-Dependent Kinase Inhibitor p27/*metabolism ; Oncogene Proteins/*metabolism ; Oxides/*pharmacology ; Transforming Growth Factor beta1/*pharmacology; Arsenic Trioxide ; Cell Line, Tumor ; Humans ; Transforming Growth Factor beta1/metabolism ; Up-Regulation
    • Abstract:
      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).
    • Accession Number:
      0 (Arsenicals)
      0 (CCNE1 protein, human)
      0 (CDKN1B protein, human)
      0 (Cyclin E)
      0 (Oncogene Proteins)
      0 (Oxides)
      0 (Transforming Growth Factor beta1)
      147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27)
      S7V92P67HO (Arsenic Trioxide)
    • Publication Date:
      Date Created: 20090225 Date Completed: 20110823 Latest Revision: 20181201
    • Publication Date:
      20221213
    • Accession Number:
      19236751