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


CONCLUSIONS
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.
Liu
Jia-Ren
JR
Public Health College, Harbin Medical University, Harbin 150001, Heilongjiang Province, China. jiarenliu@yahoo.com
Chen
Bing-Qing
BQ
Yang
Yan-Mei
YM
Wang
Xuan-Ling
XL
Xue
Ying-Ben
YB
Zheng
Yu-Mei
YM
Liu
Rui-Hai
RH
D000230:Adenocarcinoma / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D000970:Antineoplastic Agents / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D002453:Cell Cycle / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects; D006801:Humans; D019394:Ki-67 Antigen / Q000378:metabolism; D008041:Linoleic Acids / Q000494:pharmacology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D016271:Proto-Oncogene Proteins c-myc / Q000378:metabolism; D013274:Stomach Neoplasms / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D014407:Tumor Cells, Cultured; D019014:fas Receptor / Q000378:metabolism
D000970:Antineoplastic Agents; D019394:Ki-67 Antigen; D008041:Linoleic Acids; D019253:Proto-Oncogene Proteins c-bcl-2; D016271:Proto-Oncogene Proteins c-myc; D019014:fas Receptor