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Objective: To determine the effect of cis-9, trans-1 1-conjugated linoleic acid on the cell cycle of mammary cancer cells (MCF-7) and the possible mechanism of the inhibitory effect of c9,t11-CLA. 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 MCF-7 cells at various c9,t11-CLA concentrations (25mM, 50mM, 100mM and 200mM), at 24h and 48h. 96% ethand was used as negative control. Results: The cell growth and DNA synthesis of MCF-7 cells were inhibited by c9,t11-CLA. After treatment with various doses of c9,t11-CLA mentioned above for 8 days, the inhibition frequency was 27.18%, 35.43%, 91.05%, and 92.86%, respectively. Inhibitory effect of c9,t11-CLA on DNA synthesis (except for 25mM, 24h) was demonstrated by significantly less incorporation of 3H-TdR than the negative control (P<0.05 and P<0.01). To further investigate the influence of the cell cycle progression, we found that c9,t11-CLA may arrest the cell cycle of MCF-7 cells. Immunocytochemical staining demonstrated that incubation with different concentration of c9,t11-CLA at various times significantly decreased the expression of PCNA, Cyclin A, B1, D1 in MCF-7 cells compared to the negative control (P<0.01), whereas the expression of p16ink4a and p21cip/waf1, cyclin-dependent kinases inhibitors (CDKI), were increased. Conclusions: The cell growth and proliferation of MCF-7 cells is inhibited by c9,t11-CLA via blocking cell cycle, accompanying reduced expression of cyclin A, B1, D1 and enhanced expression of CDKI (p16ink4a and p21cip/wafl).
Objective: To determine the effect of cis-9, trans-1 1-conjugated linoleic acid on the cell cycle of mammary cancer cells (MCF-7) and the possible mechanism of the inhibitory effect of c9, t11-CLA. 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 MCF-7 cells at various c9, t11- CLA concentrations (25mM, 50mM, 100mM Results: The cell growth and DNA synthesis of MCF-7 cells were inhibited by c9, t11-CLA. After treatment with each dose of c9, t11- Inhibition of c9, t11-CLA on DNA synthesis (except for 25 mM, 24h) was demonstrated by significantly less incorporation of 3H-TdR than the negative control (P <0.05 and P <0.01). To further investigate the influence of the cell cycle progression , we found that c9, t11-CLA may arrest the cell cycle of MCF-7 cells. Immunocytochemical staining for that incubation with different concentration of c9, t11-CLA at various times significantly decreased the expression of PCNA, Cyclin A, B1, D1 in the MCF-7 cells compared to the negative control (P <0.01), while the expression of pl6ink4a and p21cip / waf1, cyclin-dependent kinases inhibitors (CDKI), were increased. Conclusions: The cell growth and proliferation of MCF- is inhibited by c9, t11-CLA via blocking cell cycle, accompanying reduced expression of cyclin A, B1, D1 and enhanced expression of CDKI (p16ink4a and p21cip / wafl).