DiallyldisulfidesuppressesgrowthofHL-60cellthroughincreasinghis-toneacetylationandp21WAF1expressioninvivoandinvitro

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作者
Jie ZHAOWeiguo HUANG Jie HE Hui TAN Qianjin LIAO Qi SU Cancer Research InstituteNanhua UniversityHengyang China Department of PathologyMawangdui HospitalChangsha China [2 ,3 ,2 ,2 ,2 ,2 ,2 ,4 ,2 ,421001 ,3 ,410016 ]
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关键词
diallyl disulfide; leukemia; growth inhibition; histone acetylation; p21WAF1;
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中图分类号
R733.7 [白血病];
学科分类号
100214 ;
摘要
<正> Aim:To examine the differentiation induction and growth inhibition of HL-60 cellsby diallyl disulfide(DADS),and its relationship with the alterations of histoneacetylation and p21WAF1expression in vitro and in vivo.Methods:Differentiationwas studied by nitroblue tetrazolium(NBT)reduction of HL-60 cell in vitro.HL-60cells 5×10~6 were injected into the right side of the peritoneal cavity of severecombined immunodeficiency(SCID)mice.When the peritoneal neoplasms weredetected,the SCID mice were randomly divided into 3 groups and received an ipinjection of vehicle alone(NS),DADS or sodium butyrate(SB).The growthinhibition of peritoneal neoplasms induced by DADS was observed by a growthcurve.The cycle distribution of HL-60 cells in SCID mice was monitored by flowcytometry.The expression of acetylated histone H3,H4 and p21WAF1were mea-sured by Western blot.Results:After treatment with DADS for 0-72 h,the NBTreduction ability of HL-60 cells increased in a time-dependent manner,comparedwith no treatment of HL-60 cells.In the HL-60 cells treated with DADS for 24 h,theexpression of acetylated histone H3,H4,and p21WAF1increased obviously.Aftertreatment with DADS,tumor growth was markedly suppressed.HL-60 cells frommice treated with DADS were blocked in the G1 phase,from 25.4% to 63.4%.Thetumors from the mice treated with DADS showed an increase of acetylated his-tone H3,H4,and p21WAF1.Conclusion:DADS could induce differentiation andinhibit the growth of HL-60 cells through increasing the expression of acetylatedhistone H3,I44,and p21WAF1in vitro and in vivo.
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页码:1459 / 1466
页数:8
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