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Effect of apoptosis on gastric adenocarcinoma cell line SGC-7901 induced by cis-9, trans-11-conjugated linoleic acid.

AbstractAIM:
To determine the effect of apoptosis on gastric cancer cells (SGC-7901) induced by cis-9, trans-11-conjugated linoleic acid (c9, t11-CLA) and its possible mechanism in the inhibition of cancer cells growth.
METHODS:
Using cell culture, flow cytometery and immunocytochemical techniques, we examined the cell growth, frequency of apoptosis and distribution of cell cycle, expression of ki67, bcl-2, Fas, and c-myc of SGC-7901 cells which were treated with various c9, t11-CLA concentrations (25,50,100 and 200 micromol x L(-1)) of c9, t11-CLA for 24 h and 48 h, with a negative control (0.1 % ethanol).
RESULTS:
The growth of SGC-7901 cells was inhibited by c9,t11-CLA. Eight days after treatment with various concentrations of c9,t11-CLA, as mentioned above, the inhibition rates were 5.9 %, 20.2 %,75.6 % and 82.4 %, respectively. The frequency of apoptosis on SGC-7901 cells induced by different concentrations of c9, t11-CLA (except for 25 micromol.L(-1), 24 h) was significantly greater than that in the negative control (P<0.01). To further investigate the influence of the cell cycle progression, we found that apoptosis induced by c9, t11-CLA may be involved in blocking the cell cycle of SGC-7901 cells. Immunocytochemical staining demonstrated that SGC-7901 cells preincubated in media supplemented with different c9, t11-CLA concentrations for various time periods significantly decreased the expressions of ki67 (the expression rates were 18.70-3.20 %, at 24 h and 8.10-0.20 % at 48 h, respectively), bcl-2 (4.30-0.15 % at 24 h and 8.05 %-0 at 48 h), and c-myc (4.85-2.20 % at 24 h and 4.75-0.30 % at 48 h) as compared with those in the controls (the expressions of ki67, bcl-2, and c-myc were 15.1 % at 24 h and 13.5 % at 48 h, 6.80 % at 24 h and 8.00 % at 48 h, 5.50 % at 24 h and 5.30 % at 48 h, respectively) (P<0.01), whereas the expressions of Fas were increased (0.60-2.75 %, 24 h and 0.45-5.95 %, 48 h).
CONCLUSION:
The growth and proliferation of SGC-7901 cells are inhibited by c9, t11-CLA via blocking the cell cycle, pathways of bcl-2-associated mitochondria with reduced expression of bcl-2 and Fas-associated death domain protein (FADD) with enhanced expression of Fas. But expression of c-myc on SGC-7901 cells is lower than that in negative control, which needs to be studied further.
AuthorsJia-Ren Liu, Bing-Qing Chen, Yan-Mei Yang, Xuan-Ling Wang, Ying-Ben Xue, Yu-Mei Zheng, Rui-Hai Liu
JournalWorld journal of gastroenterology (World J Gastroenterol) Vol. 8 Issue 6 Pg. 999-1004 (Dec 2002) ISSN: 1007-9327 [Print] United States
PMID12439913 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antineoplastic Agents
  • Ki-67 Antigen
  • Linoleic Acids
  • Proto-Oncogene Proteins c-bcl-2
  • Proto-Oncogene Proteins c-myc
  • fas Receptor
Topics
  • Adenocarcinoma (drug therapy, metabolism, pathology)
  • Antineoplastic Agents (pharmacology)
  • Apoptosis (drug effects)
  • Cell Cycle (drug effects)
  • Cell Division (drug effects)
  • Humans
  • Ki-67 Antigen (metabolism)
  • Linoleic Acids (pharmacology)
  • Proto-Oncogene Proteins c-bcl-2 (metabolism)
  • Proto-Oncogene Proteins c-myc (metabolism)
  • Stomach Neoplasms (drug therapy, metabolism, pathology)
  • Tumor Cells, Cultured
  • fas Receptor (metabolism)

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