Effect of cis-9, trans-11-conjugated linoleic acid on cell cycle of gastric adenocarcinoma cell line (SGC-7901).
OBJECTIVE
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, B(1), D(1), p16(ink4a) and p21(cip/waf1) of SGC-7901 cells which were treated with various c9, t11-CLA concentrations (25, 50, 100 and 200 micromol.L(-1))of c 9, t 11-CLA for 24 and 48h, 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 micromol.L, 24h) showed significantly less (3)H-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%, 24h and 9.1-0.9% at 48h, respectively), Cyclin A (11.0-2.3%, 24h and 8.5-0.5%,48h), B(1) (4.8-1.8% at 24h and 5.5-0.6% at 48h)and D(1) (3.6-1.4% at 24h and 3.7%-0 at 48h) as compared with those in the negative controls(the expressions of PCNA, Cyclin A, B(1) and D(1) were 6.5% at 24h and 9.0% at 48h, 4.2% at 24h and 5.1% at 48h, 9.5% at 24h and 6.0% at 48h,respectively)(P<0.01), whereas the expressions of P16(ink4a) and P21(cip/waf1), cyclin-dependent kinases inhibitors(CDKI), were increased.


CONCLUSIONS
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,B(1) and D(1) and enhanced expressions of CDKI(P16(ink4a) and p21(cip/waf1)).
Liu
Jia-Ren
JR
Department of Toxicological Health, Public Health College, Harbin Medical University, 199 Dongdazhi Street, Nangang District, Harbin 150001, Heilongjiang Province, China. jiarenliu@yahoo.com
Li
Bai-Xiang
BX
Chen
Bing-Qing
BQ
Han
Xiao-Hui
XH
Xue
Ying-Ben
YB
Yang
Yan-Mei
YM
Zheng
Yu-Mei
YM
Liu
Rui-Hai
RH
D000230:Adenocarcinoma / Q000473:pathology*; D000818:Animals; D002453:Cell Cycle / Q000187:drug effects*; D002455:Cell Division / Q000502:physiology; D019925:Cyclin A / Q000378:metabolism; D019926:Cyclin B / Q000378:metabolism; D056744:Cyclin B1; D019938:Cyclin D1 / Q000378:metabolism; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000378:metabolism; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D008041:Linoleic Acids / Q000737:chemistry / Q000494:pharmacology*; D044243:Linoleic Acids, Conjugated; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D013274:Stomach Neoplasms / Q000473:pathology*; D014407:Tumor Cells, Cultured
C534699:CCNB1 protein, human; C493956:CDKN1A protein, human; D019925:Cyclin A; D019926:Cyclin B; D056744:Cyclin B1; D019941:Cyclin-Dependent Kinase Inhibitor p16; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D004791:Enzyme Inhibitors; D008041:Linoleic Acids; D044243:Linoleic Acids, Conjugated; D018809:Proliferating Cell Nuclear Antigen; D019938:Cyclin D1; C046938:9,11-linoleic acid