Document Detail


Effects of allitridi on cell cycle arrest of human gastric cancer cells.
MedLine Citation:
PMID:  16222732     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
AIM: 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. CONCLUSION: 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:
Min-Wen Ha; Rui Ma; Li-Ping Shun; Yue-Hua Gong; Yuan Yuan
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  World journal of gastroenterology : WJG     Volume:  11     ISSN:  1007-9327     ISO Abbreviation:  World J. Gastroenterol.     Publication Date:  2005 Sep 
Date Detail:
Created Date:  2005-10-13     Completed Date:  2006-01-25     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100883448     Medline TA:  World J Gastroenterol     Country:  China    
Other Details:
Languages:  eng     Pagination:  5433-7     Citation Subset:  IM    
Affiliation:
Cancer Institute of the First Affiliated Hospital of China Medical University, 155 Northern Nanjing Street, Heping District, Shenyang 110001, Liaoning Province, China.
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MeSH Terms
Descriptor/Qualifier:
Adenocarcinoma, Mucinous / drug therapy,  genetics,  pathology
Allyl Compounds / pharmacology*
Antineoplastic Agents / pharmacology*
Base Sequence
Cell Cycle / drug effects
Cell Division / drug effects
Cell Line, Tumor
Cyclin-Dependent Kinase Inhibitor p21 / genetics,  metabolism
DNA, Neoplasm / genetics
Garlic
Humans
Microscopy, Electron
Stomach Neoplasms / drug therapy*,  genetics,  pathology
Sulfides / pharmacology*
Chemical
Reg. No./Substance:
0/Allyl Compounds; 0/Antineoplastic Agents; 0/CDKN1A protein, human; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/DNA, Neoplasm; 0/Sulfides; 2050-87-5/diallyl trisulfide

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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