中华胰腺病杂志
中華胰腺病雜誌
중화이선병잡지
CHINESE JOURNAL OF PANCREATOLOGY
2014年
3期
181-184
,共4页
贺志龙%夏伟%冯璜%许春芳
賀誌龍%夏偉%馮璜%許春芳
하지룡%하위%풍황%허춘방
胰腺肿瘤%二甲双胍%细胞增殖%细胞凋亡
胰腺腫瘤%二甲雙胍%細胞增殖%細胞凋亡
이선종류%이갑쌍고%세포증식%세포조망
Pancreatic neoplasms%Metformin%Cell proliferation%Apoptosis
目的 观察二甲双胍对人胰腺癌细胞株CFPAC-1增殖、凋亡的影响,探讨其相关分子机制.方法 应用1、2.5、5、10、20、40、60 mmol/L二甲双胍处理人胰腺癌CFPAC-1细胞24、48、72 h,以未处理的细胞作为对照组.采用CCK-8法检测细胞的增殖抑制率,流式细胞仪分析细胞周期,AnnexinV/PI双染法检测细胞凋亡,蛋白质印迹法检测磷酸化AMPK(p-AMPK)、FAS、cyclin D1、Bcl-xl、Bax、caspase-3、survivin蛋白的表达.结果 二甲双胍呈浓度及时间依赖性抑制CFPAC-1细胞的增殖.40 mmol/L二甲双胍处理细胞48 h后,G0/G1细胞比例显著增多[(65.93±0.27)％比(42.89±1.02)％],G2/M期、S期细胞比例显著减少[(22.01±2.95)％比(38.28±4.93)％,(13.58±0.43)％比(20.12±3.38)％],差异均有统计学意义(P值均＜0.05);细胞凋亡率从对照组的(3.01±0.49)％增加到(32.97±3.19)％(P ＜0.05);p-AMPK、Bax、caspase-3表达增强,FAS、cyclin D1、Bcl-xl、survivin表达减弱.结论 二甲双胍可以显著抑制CFPAC-1细胞增殖,促进细胞凋亡,其机制可能通过激活AMPK信号通路,下调FAS、cyclin D1、survivin表达及Bcl-xl/Bax比值,上调caspase-3表达所致.
目的 觀察二甲雙胍對人胰腺癌細胞株CFPAC-1增殖、凋亡的影響,探討其相關分子機製.方法 應用1、2.5、5、10、20、40、60 mmol/L二甲雙胍處理人胰腺癌CFPAC-1細胞24、48、72 h,以未處理的細胞作為對照組.採用CCK-8法檢測細胞的增殖抑製率,流式細胞儀分析細胞週期,AnnexinV/PI雙染法檢測細胞凋亡,蛋白質印跡法檢測燐痠化AMPK(p-AMPK)、FAS、cyclin D1、Bcl-xl、Bax、caspase-3、survivin蛋白的錶達.結果 二甲雙胍呈濃度及時間依賴性抑製CFPAC-1細胞的增殖.40 mmol/L二甲雙胍處理細胞48 h後,G0/G1細胞比例顯著增多[(65.93±0.27)％比(42.89±1.02)％],G2/M期、S期細胞比例顯著減少[(22.01±2.95)％比(38.28±4.93)％,(13.58±0.43)％比(20.12±3.38)％],差異均有統計學意義(P值均＜0.05);細胞凋亡率從對照組的(3.01±0.49)％增加到(32.97±3.19)％(P ＜0.05);p-AMPK、Bax、caspase-3錶達增彊,FAS、cyclin D1、Bcl-xl、survivin錶達減弱.結論 二甲雙胍可以顯著抑製CFPAC-1細胞增殖,促進細胞凋亡,其機製可能通過激活AMPK信號通路,下調FAS、cyclin D1、survivin錶達及Bcl-xl/Bax比值,上調caspase-3錶達所緻.
목적 관찰이갑쌍고대인이선암세포주CFPAC-1증식、조망적영향,탐토기상관분자궤제.방법 응용1、2.5、5、10、20、40、60 mmol/L이갑쌍고처리인이선암CFPAC-1세포24、48、72 h,이미처리적세포작위대조조.채용CCK-8법검측세포적증식억제솔,류식세포의분석세포주기,AnnexinV/PI쌍염법검측세포조망,단백질인적법검측린산화AMPK(p-AMPK)、FAS、cyclin D1、Bcl-xl、Bax、caspase-3、survivin단백적표체.결과 이갑쌍고정농도급시간의뢰성억제CFPAC-1세포적증식.40 mmol/L이갑쌍고처리세포48 h후,G0/G1세포비례현저증다[(65.93±0.27)％비(42.89±1.02)％],G2/M기、S기세포비례현저감소[(22.01±2.95)％비(38.28±4.93)％,(13.58±0.43)％비(20.12±3.38)％],차이균유통계학의의(P치균＜0.05);세포조망솔종대조조적(3.01±0.49)％증가도(32.97±3.19)％(P ＜0.05);p-AMPK、Bax、caspase-3표체증강,FAS、cyclin D1、Bcl-xl、survivin표체감약.결론 이갑쌍고가이현저억제CFPAC-1세포증식,촉진세포조망,기궤제가능통과격활AMPK신호통로,하조FAS、cyclin D1、survivin표체급Bcl-xl/Bax비치,상조caspase-3표체소치.
Objective To investigate the effect of metformin on the proliferation and apoptosis in human pancreatic cancer cell line CFPAC-1,and to explore the potential mechanism.Methods Human pancreatic cancer CFPAC-1 cells were cultured in vitro,and were treated with metformin at different concentrations (1,2.5,5,10,20,40,60 mmol/L) for different durations (24 h,48 h and 72 h),and cells without treatment were considered as control group.Cell proliferation was evaluated by CCK-8,cell cycle was determined by flow cytometry,apoptosis was determined by Annexin V/PI double staining method,and Western blot was used to detect the protein expression of p-AMPK,FAS,cyclin D1,Bcl-xl,Bax,caspase-3 and survivin.Results Metformin could inhibit the proliferation of CFPAC-1 cells in a time and dose dependent manner.Forty-eight hours after 40 mmol/L metformin treatment,the proportion of CFPAC-1 cells in phase G0/G1 was significantly increased [(65.93 ± 0.27)％ vs (42.89± 1.02)％],and the proportion of CFPAC-1 cells in phase G2/M,S was significantly decreased [(22.01 ± 2.95) ％ vs (38.28 ± 4.93) ％,(13.58±0.43)％ vs (20.12 ± 3.38)％],and the difference between the two groups was statistically significant (P ＜0.05).The apoptosis rate was increased from (3.01 ± 0.49) ％ to (32.97 ± 3.19) ％,(P ＜ 0.05) ; and the expression of p-AMPK,Bax,and caspase-3 was increased,while the expression of FAS,cyclin D1,Bcl-xl,survivin were decreased.Conclusions Metformin can inhibit proliferation and promote apoptosis of CFPAC-1 cells mainly by activation of AMPK pathway,and down-regulation of FAS,cyclin D1,survivin and Bcl xl/Bax ratio,as well as up-regulation of caspase-3.
