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Effect of cis-9, trans-11-conjugated linoleic acid on cell cycle of gastric adenocarcinoma cell line (SGC-7901).

AbstractAIM:
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.
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,B(1) and D(1) and enhanced expressions of CDKI(P16(ink4a) and p21(cip/waf1)).
AuthorsJia-Ren Liu, Bai-Xiang Li, Bing-Qing Chen, Xiao-Hui Han, Ying-Ben Xue, Yan-Mei Yang, Yu-Mei Zheng, Rui-Hai Liu
JournalWorld journal of gastroenterology (World J Gastroenterol) Vol. 8 Issue 2 Pg. 224-9 (Apr 2002) ISSN: 1007-9327 [Print] United States
PMID11925596 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • CCNB1 protein, human
  • CDKN1A protein, human
  • Cyclin A
  • Cyclin B
  • Cyclin B1
  • Cyclin-Dependent Kinase Inhibitor p16
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • Enzyme Inhibitors
  • Linoleic Acids
  • Linoleic Acids, Conjugated
  • Proliferating Cell Nuclear Antigen
  • Cyclin D1
  • 9,11-linoleic acid
Topics
  • Adenocarcinoma (pathology)
  • Animals
  • Cell Cycle (drug effects)
  • Cell Division (physiology)
  • Cyclin A (metabolism)
  • Cyclin B (metabolism)
  • Cyclin B1
  • Cyclin D1 (metabolism)
  • Cyclin-Dependent Kinase Inhibitor p16 (metabolism)
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins (metabolism)
  • Enzyme Inhibitors (metabolism)
  • Humans
  • Immunohistochemistry
  • Linoleic Acids (chemistry, pharmacology)
  • Linoleic Acids, Conjugated
  • Proliferating Cell Nuclear Antigen (metabolism)
  • Stomach Neoplasms (pathology)
  • Tumor Cells, Cultured

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