Tumor necrosis factor alpha: posttranscriptional stabilization of WAF1 mRNA in p53-deficient human leukemic cells.


:The p53 protein directly regulates the expression of the WAF1 (wild-type p53-activated fragment 1) protein which is a cyclin-dependent kinase inhibitor (CDK1). DNA damaging agents such as ionizing or UV radiation, and some chemical agents induce WAF1 in wild-type p53 containing cells, thereby halting cell cycle progression. WAF1 expression is also induced through a p53-independent pathway. Tumor necrosis factor alpha (TNF alpha) is a cytotoxic/cytostatic compound for some human cancer cells. We examined a series of myeloid leukemic cell lines that expressed either no p53 (HL-60, K562) or mutant inactive p53 (KG-1, KCL22,THP-1, U937). The KG-1, HL-60, K562, and KCL22 myeloid leukemic cells increased their levels of WAF1 mRNA in the presence of TNF alpha. We focused on KG-1 cells to determine how TNF alpha modulated WAF1 expression. WAF1 mRNA increased in a dose-dependent manner in the cells after exposure to increasing concentrations of TNF alpha, and this increase occurred in the absence of new protein synthesis. An increase of WAF1 protein and a concominant decrease of cyclin-dependent kinase 2 activity also was found in KG-1 cells. Flow cytometry using 5-bromo-2'-deoxyuridine showed an increase in the proportion of TNF alpha- treated KG-1 cells in the G0/G1 phase of the cell cycle. TNF alpha enhanced the rate of WAF1 transcription only 1.4 fold in TNF alpha-treated KG-1 cells as compared to untreated cells. Notably, however, the half-life (t 1/2) of WAF1 mRNA in TNF alpha-treated cells was 2.5 hours as compared to 0.5 hours in untreated cells. These results indicate that TNF alpha increases WAF1 levels at least in part via a postttranscriptional stabilization of the mRNA; and TNF alpha may mediate its cytostatic effects through WAF1 in some cell types.


J Cell Physiol


Shiohara M,Akashi M,Gombart AF,Yang R,Koeffler HP




Has Abstract


1996-03-01 00:00:00














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    authors: Fujita J,Nakayama H,Onoue H,Kanakura Y,Nakano T,Asai H,Takeda S,Honjo T,Kitamura Y

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  • Thermotolerance induced at a mild temperature of 40 degrees C protects cells against heat shock-induced apoptosis.

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    journal_title:Journal of cellular physiology

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    authors: Bettaieb A,Averill-Bates DA

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    authors: Naghizadeh S,Mohammadi A,Duijf PHG,Baradaran B,Safarzadeh E,Cho WC,Mansoori B

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    pub_type: 杂志文章


    authors: Foxall C,Wei Z,Schaefer ME,Casabonne M,Fugedi P,Peto C,Castellot JJ Jr,Brandley BK

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    journal_title:Journal of cellular physiology

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    authors: Kano-Sueoka T,Campbell GR,Gerber M

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    authors: Vali S,Carlsen R,Pessah I,Gorin F

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    journal_title:Journal of cellular physiology

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    journal_title:Journal of cellular physiology

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    journal_title:Journal of cellular physiology

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    journal_title:Journal of cellular physiology

    pub_type: 杂志文章


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    journal_title:Journal of cellular physiology

    pub_type: 杂志文章


    authors: Jia Y,Yao H,Zhou J,Chen L,Zeng Q,Yuan H,Shi L,Nan X,Wang Y,Yue W,Pei X

    更新日期:2011-11-01 00:00:00

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    journal_title:Journal of cellular physiology

    pub_type: 杂志文章


    authors: Yuan H,Li M,Feng X,Zhu E,Wang B

    更新日期:2021-03-01 00:00:00

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    journal_title:Journal of cellular physiology

    pub_type: 杂志文章,评审


    authors: Lu F,Lan Z,Xin Z,He C,Guo Z,Xia X,Hu T

    更新日期:2020-04-01 00:00:00