title: Diallyl disulfide suppresses growth of HL-60 cell through increasing histone acetylation and p21WAF1 expression in vivo and in vitro.
abstract: OBJECTIVE
  To examine the differentiation induction and growth inhibition of HL-60 cells by diallyl disulfide (DADS), and its relationship with the alterations of histone acetylation and p21(WAF1) expression in vitro and in vivo.
  
  
  METHODS
  Differentiation was studied by nitroblue tetrazolium (NBT) reduction of HL-60 cell in vitro. HL-60 cells 5x10(6) were injected into the right side of the peritoneal cavity of severe combined immunodeficiency (SCID) mice. When the peritoneal neoplasms were detected, the SCID mice were randomly divided into 3 groups and received an ip injection of vehicle alone (NS), DADS or sodium butyrate (SB). The growth inhibition of peritoneal neoplasms induced by DADS was observed by a growth curve. The cycle distribution of HL-60 cells in SCID mice was monitored by flow cytometry. The expression of acetylated histone H3, H4 and p21(WAF1) were measured by Western blot.
  
  
  RESULTS
  After treatment with DADS for 0-72 h, the NBT reduction ability of HL-60 cells increased in a time-dependent manner, compared with no treatment of HL-60 cells. In the HL-60 cells treated with DADS for 24 h, the expression of acetylated histone H3, H4, and p21(WAF1) increased obviously. After treatment with DADS, tumor growth was markedly suppressed. HL-60 cells from mice treated with DADS were blocked in the G1 phase, from 25.4% to 63.4%. The tumors from the mice treated with DADS showed an increase of acetylated histone H3, H4, and p21(WAF1).
  
  
  CONCLUSIONS
  DADS could induce differentiation and inhibit the growth of HL-60 cells through increasing the expression of acetylated histone H3, H4, and p21(WAF1) in vitro and in vivo.
authors.affiliation: Cancer Research Institute, Nanhua University, Hengyang 421001, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Zhao
authors.forename: Wei-guo
authors.initials: WG
authors.lastname: Huang
authors.forename: Jie
authors.initials: J
authors.lastname: He
authors.forename: Hui
authors.initials: H
authors.lastname: Tan
authors.forename: Qian-jin
authors.initials: QJ
authors.lastname: Liao
authors.forename: Qi
authors.initials: Q
authors.lastname: Su
mesh_terms: D000107:Acetylation / Q000187:drug effects; D000498:Allyl Compounds / Q000302:isolation & purification / Q000494:pharmacology*; D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D002453:Cell Cycle; D002454:Cell Differentiation; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000378:metabolism*; D004220:Disulfides / Q000302:isolation & purification / Q000494:pharmacology*; D005737:Garlic / Q000737:chemistry; D018922:HL-60 Cells; D006657:Histones / Q000378:metabolism*; D006801:Humans; D051379:Mice; D016513:Mice, SCID; D009368:Neoplasm Transplantation; D010534:Peritoneal Neoplasms / Q000378:metabolism* / Q000473:pathology; D011897:Random Allocation
chemical_list: D000498:Allyl Compounds; D000970:Antineoplastic Agents; C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D004220:Disulfides; D006657:Histones; C028009:diallyl disulfide