title: Effects of allitridi on cell cycle arrest of human gastric cancer cells.
abstract: OBJECTIVE
  To determine the effect of allitridi on cell cycle of human gastric cancer (HGC) cell lines MGC803 and SGC7901 and its possible mechanism.
  
  
  METHODS
  Trypan blue dye exclusion was used to evaluate the proliferation, inhibition of cells and damages of these cells were detected with electron microscope. Flow cytometry and cell mitotic index were used to analyze the change of cell cycle, immunohistochemistry, and RT-PCR was used to examine expression of the p21(WAF1) gene.
  
  
  RESULTS
  MGC803 cell growth was inhibited by allitridi with 24 h IC50 being 6.4 microg/mL. SGC7901 cell growth was also inhibited by allitridi with 24 h IC50 being 7.3 microg/mL. After being treated with allitridi at the concentration of 12 microg/mL for 24 h, cells were found to have direct cytotoxic effects, including broken cellular membrane, swollen and vesiculated mitochondria and rough endoplasmic reticula, and mass lipid droplet. When cells were treated with allitridi at the concentration of 3, 6, and 9 microg/mL for 24 h, the percentage of G0/G1 phase cells was decreased and that of G2/M phase cells was significantly increased (P = 0.002) compared with those in the group. When cells were treated with allitridi at the concentration of 6 microg/mL, cell mitotic index was much higher (P = 0.003) than that of control group, indicating that allitridi could cause gastric cancer cell arrest in M phase. Besides, the expression levels of p21(WAF1) gene of MGC803 cells and p21(WAF1) gene of SGC7901 cells were remarkably upregulated after treatment.
  
  
  CONCLUSIONS
  Allitridi can cause gastric cancer cell arrest in M phase, and this may be one of the mechanisms for inhibiting cell proliferation. Effect of allitridi on cells in M phase may be associated with the upregulation of p21(WAF1) genes. This study provides experimental data for clinical use of allitridi in the treatment of gastric carcinoma.
authors.affiliation: Cancer Institute of the First Affiliated Hospital of China Medical University, 155 Northern Nanjing Street, Heping District, Shenyang 110001, Liaoning Province, China.
authors.forename: Min-Wen
authors.initials: MW
authors.lastname: Ha
authors.forename: Rui
authors.initials: R
authors.lastname: Ma
authors.forename: Li-Ping
authors.initials: LP
authors.lastname: Shun
authors.forename: Yue-Hua
authors.initials: YH
authors.lastname: Gong
authors.forename: Yuan
authors.initials: Y
authors.lastname: Yuan
mesh_terms: D002288:Adenocarcinoma, Mucinous / Q000188:drug therapy / Q000235:genetics / Q000473:pathology; D000498:Allyl Compounds / Q000494:pharmacology*; D000970:Antineoplastic Agents / Q000494:pharmacology*; D001483:Base Sequence; D002453:Cell Cycle / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects; D045744:Cell Line, Tumor; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000235:genetics / Q000378:metabolism; D004273:DNA, Neoplasm / Q000235:genetics; D005737:Garlic; D006801:Humans; D008854:Microscopy, Electron; D013274:Stomach Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D013440:Sulfides / Q000494:pharmacology*
chemical_list: D000498:Allyl Compounds; D000970:Antineoplastic Agents; C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D004273:DNA, Neoplasm; D013440:Sulfides; C042577:diallyl trisulfide