title: Effect of diallyl disulfide on cell cycle arrest of human colon cancer SW480 cells.
abstract: OBJECTIVE
  Our previous study revealed that diallyl disulfide (DADS) significantly inhibited cell proliferation and induced cell cycle arrest at G(2)/M phase of human colon cancer SW480 cells. However, the molecular mechanism of cell cycle arrest remains unclear. This study was to investigate the role and the molecular mechanism of DADS in the induction of cell cycle arrest of human colon cancer cell line SW480.
  
  
  METHODS
  Proliferation of SW480 cells after DADS treatment was measured by MTT assay and cell counting. Phase distribution of cell cycle was analyzed by flow cytometry. Expressions of PCNA, p53, p21(WAF1) and cyclin B1 were detected by immunohistochemistry and western blot.
  
  
  RESULTS
  DADS (30-70 microg/mL) significantly inhibited proliferation and retarded the population doubling time of colonies in SW480 cells. Compared with the control group, SW480 cells were markedly accumulated at G(2)/M phase after the treatment with DADS (p < 0.05). Moreover, DADS remarkably decreased the protein contents of PCNA, p53 and cyclin B1, but increased the expression of p21(WAF1) in a time- and dose-dependent manner.
  
  
  CONCLUSIONS
  DADS induces G(2)/M arrest in human colon cancer SW480 cells, probably through the downregulation of PCNA, p53 and cyclin B1 and upregulation of p21(WAF1).
authors: Cancer Research Institute, The Second Affiliated Hospital, University of South China, Hengyang, Hunan, PR China.
authors: Qian-Jin
authors: QJ
authors: Liao
authors: Jian
authors: J
authors: Su
authors: Jie
authors: J
authors: He
authors: Ying
authors: Y
authors: Song
authors: Hai-Lin
authors: HL
authors: Tang
authors: Qi
authors: Q
authors: Su
mesh_terms: D000498:Allyl Compounds / Q000494:pharmacology*; D015153:Blotting, Western; D002453:Cell Cycle / Q000187:drug effects*; D002455:Cell Division / Q000187:drug effects; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects*; D003110:Colonic Neoplasms / Q000378:metabolism / Q000473:pathology; D019938:Cyclin D1 / Q000378:metabolism; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000378:metabolism; D004220:Disulfides / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005434:Flow Cytometry; D016195:G2 Phase / Q000235:genetics; D006801:Humans; D007150:Immunohistochemistry; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D013997:Time Factors; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D000498:Allyl Compounds; C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D004220:Disulfides; D018809:Proliferating Cell Nuclear Antigen; D016159:Tumor Suppressor Protein p53; D019938:Cyclin D1; C028009:diallyl disulfide