抑制JNK通路对Genistein诱导结肠癌SW620细胞周期阻滞的作用(1)
[摘要] 目的 探讨染料木黄酮(Genistein，Gen)阻滞结肠癌细胞S期向G2/M期转换与JNK通路的关系。 方法 以人结肠癌SW620细胞为研究对象，实验分三个系列组，第一系列组为对照组和SP600125组(10 μmol/L、20 μmol/L、30 μmol/L、40 μmol/L)，第二系列为对照组、Gen组(20 μmol/L、40 μmol/L、80 μmol/L)和联用组(Gen 40 μmol/L和SP600125 40 μmol/L)，第三系列为对照组、Gen组(40 μmol/L)、SP600125组(40 μmol/L)和联用组。蛋白质印迹法筛选SP600125的最适工作浓度及Cyclin B1、P-Cdc2和Cdc2蛋白的表达。MTS法检测细胞增殖。 结果 SP600125的最适工作浓度为40 μmol/L。药物组的Cyclin B1(除Gen 20 μmol/L组)、P-Cdc2和Cdc2蛋白表达均显著下调(P<0.01)，Cyclin B1蛋白表达随Gen剂量的增加而降低(P<0.01)，联用组Cyclin B1明显低于Gen 40 μmol/L组(P<0.01)，联用组P-Cdc2和Cdc2蛋白与Gen 40 μmol/L组的比较虽有降低的趋势，但差异无统计学意义(P>0.05)。抑制JNK通路可增强Gen抗SW620细胞增殖的作用。 结论 抑制JNK通路可通过减少结肠癌SW620细胞Cyclin B1-Cdc2的活化，阻滞细胞由S期进入G2/M期。
[關键词] 染料木黄酮;JNK;结肠癌;细胞周期
[中图分类号] R329 [文献标识码] A [文章编号] 1673-9701(2019)34-0026-05
Effect of inhibition of JNK pathway on Genistein-induced colon cancer SW620 cell cycle arrest
LANG Huiling1 LIU Shengnan1 QIAN Tiantian1 CAO Di1 WANG Yusu2 YU Jiaqi1 ZHAO Zhongxin3 LIU Dan1
1.Qiqihar Medical University， Qiqihar 161006，China;2.Harbin Medical University， Harbin 150081，China;3.Department of General Surgery， the First Affiliated Hospital of Qiqihar Medical University， Qiqihar 161041，China
[Abstract] Objective To investigate the relationship between genistein(Genstein， Gen)-induced colon cancer cell arrest from S phase into G2/M phase and JNK pathway. Methods Human colon cancer SW620 cells were used as the research object. The cells were divided into three series. The first series were the control group and the SP600125 group (10 μmol/L， 20 μmol/L， 30 μmol/L， 40 μmol/L). The second series were the control group， the Gen group (20 μmol/L， 40 μmol/L， 80 μmol/L) and the combination group(Gen 40 μmol/L and SP600125 40 μmol/L). The third series were the control group， the Gen group (40 μmol/L)， the SP600125 group (40 μmol/L) and the combination group. Western blotting was used to screen the optimal working concentration of SP600125 and the expression of Cyclin B1， P-Cdc2 and Cdc2 proteins. Cell proliferation was detected by the MTS method. Results The optimum working concentration of SP600125 was determined as 40 μmol/L. The expression of Cyclin B1(except for Gen 20 μmol/L group)， P-Cdc2 and Cdc2 protein in the drug group was significantly reduced(P<0.01). The expression of Cyclin B1 protein was decreased with the increase of Gen dose (P<0.01). The Cyclin B1 of the combination group was significantly lower than that of the Gen 40 μmol/L group (P<0.01). A decreasing trend of P-Cdc2 and Cdc2 proteins was found in the combination group compared with the Gen 40 μmol/L group， but the difference was statistical insignificant (P>0.05). The proliferation of Gen anti-SW620 cells was enhanced by the inhibition of JNK pathway. Conclusion Inhibition of JNK pathway can inhibit the activation of Cyclin B1-Cdc2 in colon cancer SW620 cells， block cells in S phase and prevent cells entering into G2/M phase., http://www.100md.com(郎慧玲 刘晟男 钱甜甜 曹玓 王钰粟 于佳琪 赵忠新 刘丹)
[關键词] 染料木黄酮;JNK;结肠癌;细胞周期
[中图分类号] R329 [文献标识码] A [文章编号] 1673-9701(2019)34-0026-05
Effect of inhibition of JNK pathway on Genistein-induced colon cancer SW620 cell cycle arrest
LANG Huiling1 LIU Shengnan1 QIAN Tiantian1 CAO Di1 WANG Yusu2 YU Jiaqi1 ZHAO Zhongxin3 LIU Dan1
1.Qiqihar Medical University， Qiqihar 161006，China;2.Harbin Medical University， Harbin 150081，China;3.Department of General Surgery， the First Affiliated Hospital of Qiqihar Medical University， Qiqihar 161041，China
[Abstract] Objective To investigate the relationship between genistein(Genstein， Gen)-induced colon cancer cell arrest from S phase into G2/M phase and JNK pathway. Methods Human colon cancer SW620 cells were used as the research object. The cells were divided into three series. The first series were the control group and the SP600125 group (10 μmol/L， 20 μmol/L， 30 μmol/L， 40 μmol/L). The second series were the control group， the Gen group (20 μmol/L， 40 μmol/L， 80 μmol/L) and the combination group(Gen 40 μmol/L and SP600125 40 μmol/L). The third series were the control group， the Gen group (40 μmol/L)， the SP600125 group (40 μmol/L) and the combination group. Western blotting was used to screen the optimal working concentration of SP600125 and the expression of Cyclin B1， P-Cdc2 and Cdc2 proteins. Cell proliferation was detected by the MTS method. Results The optimum working concentration of SP600125 was determined as 40 μmol/L. The expression of Cyclin B1(except for Gen 20 μmol/L group)， P-Cdc2 and Cdc2 protein in the drug group was significantly reduced(P<0.01). The expression of Cyclin B1 protein was decreased with the increase of Gen dose (P<0.01). The Cyclin B1 of the combination group was significantly lower than that of the Gen 40 μmol/L group (P<0.01). A decreasing trend of P-Cdc2 and Cdc2 proteins was found in the combination group compared with the Gen 40 μmol/L group， but the difference was statistical insignificant (P>0.05). The proliferation of Gen anti-SW620 cells was enhanced by the inhibition of JNK pathway. Conclusion Inhibition of JNK pathway can inhibit the activation of Cyclin B1-Cdc2 in colon cancer SW620 cells， block cells in S phase and prevent cells entering into G2/M phase., http://www.100md.com(郎慧玲 刘晟男 钱甜甜 曹玓 王钰粟 于佳琪 赵忠新 刘丹)