AIM: 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.METHOD...AIM: 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 μmol@L-1) of c9, t11-CLA for 24h 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 μmol@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), bd-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-mycwere 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).CONCLUSION: The growth and proliferation of SGC-7901 cells are inhibited by cg, 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.展开更多
AIM: To explore the inhibition of conjugated linoleic acidisomers in different purity (75 % purity c9,t11-, 98 % purityc9,t11- and 98 % purity t10,c12-CLA) on the formation offorestomach neoplasm and cheopreventive me...AIM: To explore the inhibition of conjugated linoleic acidisomers in different purity (75 % purity c9,t11-, 98 % purityc9,t11- and 98 % purity t10,c12-CLA) on the formation offorestomach neoplasm and cheopreventive mechanisms.METHODS: Forestomach neoplasm model induced by B(a)P in KunMing mice was established. The numbers of tumorand diameter of each tumor in forestomach were counted;the mice plasma malondialdehyde (MDA) were measuredby TBARS assay; TUNEL assay was used to analyze theapoptosis in forestomach neoplasia and the expression ofMEK-1, ERK-1, MKP-1 protein in forestomach neoplasm werestudied by Western Blotting assay.RESULTS: The incidence of neoplasm in B(a)P group, 75 %purity c9, t11-CLA group, 98 % purity cg,t11-CLA groupand 98 % purity t10, c12-CLA group was 100 %, 75.0 %(P＞0.05), 69.2 % (P＜0.05) and 53.8 % (P＜0.05) respectivelyand the effect of two CLA isomers in 98 % purity onforestomach neoplasia was significant; CLA showed noinfluence on the average tumor numbers in tumor-bearingmouse, but significantly decreased the tumor size, the tumoraverage diameter of mice in 75 % purity c9,t11-CLA group,98 % purity cg,t11-CLA group and 98 % purity t10, c12-CLAgroup was 0.157±0.047 cm, 0.127±0.038 cm and 0.128±0.077 cm (P＜0.05) and 0.216±0.088 cm in B(a)P group;CLA could also significantly increase the apoptosis cellnumbers by 144.00±20.31, 153.75±23.25, 157.25±15.95(P＜0.05) in 75 % purity c9,t11-CLA group, 98 % purity c9,t11-CLA group and 98 % purity t10,c12-CLA group (30.88±3.72 in BP group); but there were no significant differencesbetween the effects of 75 % purity c9,t11-CLA and twoisomers in 98 % purity on tumor size and apoptotic cellnumbers; the plasma levels of MDA in were increased by75 % purity c9,t11-ClA, 98 % purity c9,t11-CLA and 98 %purity t10,c12-CLA. The 75 % purity c9,t11-CLA showedstronger inhibition; CLA could also inhibit the expression ofERK-1 protein and promote the expression of MKP-1 protein,however no influence of CLA on MEK-1 protein was observed.CONCLUSION: Two isomers in 98 % purity show strongerinhibition on carcinogenesis. However, the inhibitorymechanisms of CLA on carcinogenesis is complicated, whichmay be due to the increased mice plasmaMDA, the inducingapoptosis in tumor tissues. And the effect of CLA on theexpression of ERK-1 and MKP-1 may be one of themechanisms of the inhibition of CLA on the tumor.展开更多
AIM: To investigate the effect of c9, t11-conjugated linoleic acid (c9,t11-CLA) on the adhesion of human gastric carcinoma cell line (SGC-7901).METHODS: SGC-7901 cells were at first treated with different concentratio...AIM: To investigate the effect of c9, t11-conjugated linoleic acid (c9,t11-CLA) on the adhesion of human gastric carcinoma cell line (SGC-7901).METHODS: SGC-7901 cells were at first treated with different concentrations (25, 50, 100, 200 μmol/L) of c9,t111-CLA and 1 mL/L ethanol (as a negative control) for 24 h.Using adhesion assay and Western blot, we investigated the ability of SGC-7901 cells to adhere to intracellular matrix and examined the expression of E-cadherin (ECD), α-catenin,intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in these cells.RESULTS: The attachment rate to laminin of SGC-7901 cells treated with different concentrations of c9,t11-CLA (0,25, 50, 100, and 200 μmol/L) was 100.0±3.3, 95.7±4.0,89.2±4.6, 87.9±6.1, and 65.9±5.8, respectively. The attachment rate to fibronectin was 100.0±4.7, 96.8±3.8,94.5±4.1, 76.5±4.3, and 61.8±4.8, respectively. The attachment rate to Matrigel was 99.9±6.6, 91.4±6.8,85.5±7.4, 79.3±5.6, and 69.6±5.1, respectively. Besides,c9,t11-CLA could increase the level of ECD and α-catenin,and decrease the level of ICAM-1 and VCAM-1 in SGC-7901 cells.CONCLUSION: c9, t11-CLA can reduce the adhesion of human gastric carcinoma cells to laminin, fibronectin and Matrigel. c9,t11-CLA can increase the level of ECD and α-catenin, and decrease the level of ICAM-1 and VCAM-1 in human gastric carcinoma cells.展开更多
基金the National Natural Science Foundation of China,No.39870661
文摘AIM: 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 μmol@L-1) of c9, t11-CLA for 24h 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 μmol@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), bd-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-mycwere 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).CONCLUSION: The growth and proliferation of SGC-7901 cells are inhibited by cg, 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.
基金the National Natural Science Foundation ot China, No.30070658
文摘AIM: To explore the inhibition of conjugated linoleic acidisomers in different purity (75 % purity c9,t11-, 98 % purityc9,t11- and 98 % purity t10,c12-CLA) on the formation offorestomach neoplasm and cheopreventive mechanisms.METHODS: Forestomach neoplasm model induced by B(a)P in KunMing mice was established. The numbers of tumorand diameter of each tumor in forestomach were counted;the mice plasma malondialdehyde (MDA) were measuredby TBARS assay; TUNEL assay was used to analyze theapoptosis in forestomach neoplasia and the expression ofMEK-1, ERK-1, MKP-1 protein in forestomach neoplasm werestudied by Western Blotting assay.RESULTS: The incidence of neoplasm in B(a)P group, 75 %purity c9, t11-CLA group, 98 % purity cg,t11-CLA groupand 98 % purity t10, c12-CLA group was 100 %, 75.0 %(P＞0.05), 69.2 % (P＜0.05) and 53.8 % (P＜0.05) respectivelyand the effect of two CLA isomers in 98 % purity onforestomach neoplasia was significant; CLA showed noinfluence on the average tumor numbers in tumor-bearingmouse, but significantly decreased the tumor size, the tumoraverage diameter of mice in 75 % purity c9,t11-CLA group,98 % purity cg,t11-CLA group and 98 % purity t10, c12-CLAgroup was 0.157±0.047 cm, 0.127±0.038 cm and 0.128±0.077 cm (P＜0.05) and 0.216±0.088 cm in B(a)P group;CLA could also significantly increase the apoptosis cellnumbers by 144.00±20.31, 153.75±23.25, 157.25±15.95(P＜0.05) in 75 % purity c9,t11-CLA group, 98 % purity c9,t11-CLA group and 98 % purity t10,c12-CLA group (30.88±3.72 in BP group); but there were no significant differencesbetween the effects of 75 % purity c9,t11-CLA and twoisomers in 98 % purity on tumor size and apoptotic cellnumbers; the plasma levels of MDA in were increased by75 % purity c9,t11-ClA, 98 % purity c9,t11-CLA and 98 %purity t10,c12-CLA. The 75 % purity c9,t11-CLA showedstronger inhibition; CLA could also inhibit the expression ofERK-1 protein and promote the expression of MKP-1 protein,however no influence of CLA on MEK-1 protein was observed.CONCLUSION: Two isomers in 98 % purity show strongerinhibition on carcinogenesis. However, the inhibitorymechanisms of CLA on carcinogenesis is complicated, whichmay be due to the increased mice plasmaMDA, the inducingapoptosis in tumor tissues. And the effect of CLA on theexpression of ERK-1 and MKP-1 may be one of themechanisms of the inhibition of CLA on the tumor.
基金Supported by the National Natural Science Foundation of China,No.30070658
文摘AIM: To investigate the effect of c9, t11-conjugated linoleic acid (c9,t11-CLA) on the adhesion of human gastric carcinoma cell line (SGC-7901).METHODS: SGC-7901 cells were at first treated with different concentrations (25, 50, 100, 200 μmol/L) of c9,t111-CLA and 1 mL/L ethanol (as a negative control) for 24 h.Using adhesion assay and Western blot, we investigated the ability of SGC-7901 cells to adhere to intracellular matrix and examined the expression of E-cadherin (ECD), α-catenin,intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in these cells.RESULTS: The attachment rate to laminin of SGC-7901 cells treated with different concentrations of c9,t11-CLA (0,25, 50, 100, and 200 μmol/L) was 100.0±3.3, 95.7±4.0,89.2±4.6, 87.9±6.1, and 65.9±5.8, respectively. The attachment rate to fibronectin was 100.0±4.7, 96.8±3.8,94.5±4.1, 76.5±4.3, and 61.8±4.8, respectively. The attachment rate to Matrigel was 99.9±6.6, 91.4±6.8,85.5±7.4, 79.3±5.6, and 69.6±5.1, respectively. Besides,c9,t11-CLA could increase the level of ECD and α-catenin,and decrease the level of ICAM-1 and VCAM-1 in SGC-7901 cells.CONCLUSION: c9, t11-CLA can reduce the adhesion of human gastric carcinoma cells to laminin, fibronectin and Matrigel. c9,t11-CLA can increase the level of ECD and α-catenin, and decrease the level of ICAM-1 and VCAM-1 in human gastric carcinoma cells.
