Gastric Cancer
Copyright ©The Author(s) 2002. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Apr 15, 2002; 8(2): 224-229
Published online Apr 15, 2002. doi: 10.3748/wjg.v8.i2.224
Effect of cis-9, trans-11-conjugated linoleic acid on cell cycle of gastric adenocarcinoma cell line (SGC-7901)
Jia-Ren Liu, Bai-Xiang Li, Bing-Qing Chen, Xiao-Hui Han, Ying-Ben Xue, Yan-Mei Yang, Yu-Mei Zheng, Rui-Hai Liu
Jia-Ren Liu, Bai-Xiang Li, Bing-Qing Chen, Yan-Mei Yang, Yu-Mei Zheng, Ying-ben Xue, Department of Toxicological Health, Public Health College, Harbin Medical University, Harbin 150001, Heilongjiang Province, China
Xiao-Hui Han, ICU of Cardiological Surgery, The Second Hospital, Harbin Medical University, Harbin 150001, Heilongjiang Province, China
Rui-Hai Liu, Food Science and Toxicology, Department of Food Science, Cornell University, Ithaca, NY 14853-7201, USA
Author contributions: All authors contributed equally to the work.
Supported by the National Natural Science Foundation of China, No. 39870661
Correspondence to: Dr. Jia-ren Liu, 199 Dongdazhi Street, Nangang District, Harbin 150001, Heilongjiang Province, China.jiarenliu@yahoo.com
Telephone: +86-451-3639459 Fax: +86-451-3641253
Received: August 23, 2001
Revised: September 1, 2001
Accepted: September 5, 2001
Published online: April 15, 2002
Abstract

AIM: To determine the effect of cis-9, trans-11-conjugated linoleic acid (c9,t11-CLA) on the cell cycle of gastric cancer cells (SGC-7901) and its possible mechanism in inhibition cancer growth.

METHODS: Using cell culture and immunocytochemical techniques, we examined the cell growth, DNA synthesis, expression of PCNA, cyclin A, B1, D1, P16ink4a and P21cip/waf1 of SGC-7901 cells which were treated with various c9,t11-CLA concentrations (25, 50, 100 and 200 μmol•L⁻¹)of c9,t11-CLA for 24 and 48 h, with a negative control (0.1% ethane).

RESULTS: The cell growth and DNA synthesis of SGC-7901 cells were inhibited by c9,t11-CLA. SGC-7901 cells. Eight day after treatment with various concentrations of c9,t11-CLA mentioned above, the inhibition rates were 5.92%, 20.15%, 75.61% and 82.44%, respectively and inhibitory effect of c9,t11-CLA on DNA synthesis (except for 25 μmol/L, 24 h) showed significantly less 3H-TdR incorporation than that in the negative controls (P < 0.05 and P < 0.01). Immunocytochemical staining demonstrated that SGC-7901 cells preincubated in media supplemented with different c9,t11-CLA concentrations at various times significantly decreased the expressions of PCNA (the expression rates were 7.2%-3.0%, 24 h and 9.1%-0.9% at 48 h, respectively), Cyclin A (11.0%-2.3%, 24 h and 8.5%-0.5%, 48 h), B1 (4.8%-1.8% at 24 h and 5.5%-0.6% at 48 h)and D1 (3.6%-1.4% at 24 h and 3.7%-0% at 48 h) as compared with those in the negative controls (the expressions of PCNA, Cyclin A, B1 and D1 were 6.5% at 24 h and 9.0% at 48 h, 4.2% at 24 h and 5.1% at 48 h, 9.5% at 24 h and 6.0% at 48 h, respectively) (P < 0.01), whereas the expressions of P16ink4a and P21cip/waf1, cyclin-dependent kinases inhibitors (CDKI), were increased.

CONCLUSION: The cell growth and proliferation of SGC-7901 cell is inhibited by c9,t11-CLA via blocking the cell cycle, with reduced expressions of cyclin A, B1 and D1 and enhanced expressions of CDKI (P16ink4a and P21cip/waf1).

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