中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2015年
4期
715-717
,共3页
蓝球生%曾育杰%许鹤洋%张旸%李守峰%褚忠华
藍毬生%曾育傑%許鶴洋%張旸%李守峰%褚忠華
람구생%증육걸%허학양%장양%리수봉%저충화
结直肠癌%扭曲肉芝甲酯%细胞迁移%脱噬作用
結直腸癌%扭麯肉芝甲酯%細胞遷移%脫噬作用
결직장암%뉴곡육지갑지%세포천이%탈서작용
Colorectal cancer%Methyl sartortuoate%Cell migration%Apoptosis
目的 观察扭曲肉芝甲酯对人结肠癌细胞侵袭、迁移的抑制作用.方法 随机将LoVo细胞分为对照组和处理组(10、30、50 μmol/L),扭曲肉芝甲酯处理LoVo细胞后对凋亡率、迁移能力、凋亡信号通路蛋白改变进行测定.结果 经10、30、50 μmol/L扭曲肉芝甲酯处理24 h后,LoVo细胞凋亡率分别为(2.30±0.93)％、(11.03±0.14)％和(16.29±1.98)％,对照组凋亡率为(2.09±0.97)％,而50μmol/L扭曲肉芝甲酯处理0、6、12、24h后凋亡率分别为(2.67±0.97)％、(5.08±1.03)％、(5.04±0.83)％和(13.50±1.16)％(P＜0.05);利用Transwell小室检测提示扭曲肉芝甲酯可抑制结肠癌细胞的迁移、侵袭(P＜0.05).Western blot法结果显示扭曲肉芝甲酯处理后结肠癌细胞磷酸化的c-Jun氨基末端激酶(JNK)、p38蛋白升高(P＜0.05).结论 扭曲肉芝甲酯通过激活凋亡信号通路丝裂原活化蛋白激酶(MAPK),从而诱导结肠癌细胞的凋亡,并进一步抑制结肠癌细胞的迁移、侵袭.
目的 觀察扭麯肉芝甲酯對人結腸癌細胞侵襲、遷移的抑製作用.方法 隨機將LoVo細胞分為對照組和處理組(10、30、50 μmol/L),扭麯肉芝甲酯處理LoVo細胞後對凋亡率、遷移能力、凋亡信號通路蛋白改變進行測定.結果 經10、30、50 μmol/L扭麯肉芝甲酯處理24 h後,LoVo細胞凋亡率分彆為(2.30±0.93)％、(11.03±0.14)％和(16.29±1.98)％,對照組凋亡率為(2.09±0.97)％,而50μmol/L扭麯肉芝甲酯處理0、6、12、24h後凋亡率分彆為(2.67±0.97)％、(5.08±1.03)％、(5.04±0.83)％和(13.50±1.16)％(P＜0.05);利用Transwell小室檢測提示扭麯肉芝甲酯可抑製結腸癌細胞的遷移、侵襲(P＜0.05).Western blot法結果顯示扭麯肉芝甲酯處理後結腸癌細胞燐痠化的c-Jun氨基末耑激酶(JNK)、p38蛋白升高(P＜0.05).結論 扭麯肉芝甲酯通過激活凋亡信號通路絲裂原活化蛋白激酶(MAPK),從而誘導結腸癌細胞的凋亡,併進一步抑製結腸癌細胞的遷移、侵襲.
목적 관찰뉴곡육지갑지대인결장암세포침습、천이적억제작용.방법 수궤장LoVo세포분위대조조화처리조(10、30、50 μmol/L),뉴곡육지갑지처리LoVo세포후대조망솔、천이능력、조망신호통로단백개변진행측정.결과 경10、30、50 μmol/L뉴곡육지갑지처리24 h후,LoVo세포조망솔분별위(2.30±0.93)％、(11.03±0.14)％화(16.29±1.98)％,대조조조망솔위(2.09±0.97)％,이50μmol/L뉴곡육지갑지처리0、6、12、24h후조망솔분별위(2.67±0.97)％、(5.08±1.03)％、(5.04±0.83)％화(13.50±1.16)％(P＜0.05);이용Transwell소실검측제시뉴곡육지갑지가억제결장암세포적천이、침습(P＜0.05).Western blot법결과현시뉴곡육지갑지처리후결장암세포린산화적c-Jun안기말단격매(JNK)、p38단백승고(P＜0.05).결론 뉴곡육지갑지통과격활조망신호통로사렬원활화단백격매(MAPK),종이유도결장암세포적조망,병진일보억제결장암세포적천이、침습.
Objective To investigate the underlying mechanisms of methyl sartortuoate inhibiting invasion and migration of human colon cancer cells.Methods LoVo cells were randomly divided into control and methyl sartortuoate-treated (10,30,and 50 μmol/L) groups.The apoptosis rate,migration,and apoptosis proteins expression changes were analyzed.Results The methyl sartortuoate in a certain concentration range inhibited the growth of LoVo and DLD-1 cells in a concentration-and time-dependent manner (P ＜0.05).After treatment with methyl sartortuoate (0,10,30 and 50 μmol/L) for 24 h,the apoptosis rate of LoVo cell was (2.09 ±0.97)％,(2.32 ±0.93)％,(11.03 ±0.14)％ and (16.29 ± 1.98)％ respectively.After treatment with 50 μmol/L methyl sartortuoate for 0,6,12,or 24h,theapoptosis rate was (2.67 ±0.97)％,(5.08±1.03)％,(5.04 ±0.83)％ and (13.50 ± 1.16) ％ (P ＜ 0.05) respectively.Transwell invasion assay indicated that methyl sartortuoate could inhibit invasion and migration of colon cancer LoVo cells.Western blotting results showed that phospho-c-Jun N-terminal kinase (JNK) and phospho-38 expression was up-regulated in LoVo cells treated with methyl sartortuoate.Conclusion The results indicated that methyl sartortuoate could induce apoptosis by activating mitogen-activated protein kinase (MAPK)/JNK and P38 signaling,and further inhibit the migration and invasion of LoVo cells.
