中华肝胆外科杂志
中華肝膽外科雜誌
중화간담외과잡지
CHINESE JOURNAL OF HEPATOBILIARY SURGERY
2012年
12期
933-937
,共5页
李鹏%刘江伟%韩振魁%斯坎德尔·努尔买买提%许永华%张燕%杨珍珍%董翔
李鵬%劉江偉%韓振魁%斯坎德爾·努爾買買提%許永華%張燕%楊珍珍%董翔
리붕%류강위%한진괴%사감덕이·노이매매제%허영화%장연%양진진%동상
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 研究二甲双胍在体外对人胰腺癌细胞BxPC 3、AsPC 1生长增殖、凋亡的影响及其抗肿瘤相关分子机制.方法 体外培养人胰腺癌BxPC-3、AsPC 1细胞,四甲基偶氮唑盐(MTT)法检测二甲双胍在不同浓度和不同时间对于胰腺癌细胞增殖的影响,并计算IC50值.用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记测定(TUNEL)法检测处理后细胞的凋亡情况.RT-PCR法检测COX-2、bcl-2、Survivin的表达影响.结果 MTT法检测显示,不同浓度二甲双胍均可抑制BxPC-3、AsPC-1两种人胰腺癌细胞增殖,两种胰腺癌细胞IC50分别为68.882 mmol/L和90.984 mmol/L.TUNEL法检测人胰腺癌细胞BxPC-3,正常对照组及二甲双胍干预组(以1/2 IC50浓度处理胰腺癌细胞)凋亡率分别为(2.44±0.57)％和(17.52±0.75)％,P＜0.05；胰腺癌细胞AsPC-1在正常对照组及二甲双胍干预组凋亡率分别为(5.35±0.92)％和(45.76±1.87)％,P＜0.05.RT-PCR结果显示:人胰腺癌细胞BxPC-3在正常对照组及二甲双胍干预组COX-2的mRNA灰度值分别为0.769±0.006和0.305±0.009,P＜0.05； bcl-2的mRNA灰度值分别为0.401±0.022和0.129±0.010,P＜0.05；Survivin的mRNA灰度值分别为0.943±0.029和0.143±0.050,P＜0.05.人胰腺癌AsPC-1细胞在正常对照组及二甲双胍干预组COX-2的mRNA灰度值分别为1.232±0.011和0.831±0.022,P＜0.05；bcl-2的mRNA灰度值分别为0.400±0.053和0.129±0.032,P＜0.05；Survivin的mRNA灰度值分别为0.983±0.017和0.174±0.029,P＜0.05.结论 二甲双胍抑制胰腺癌细胞增殖、促进凋亡.二甲双胍抗肿瘤机制可能是通过抑制COX-2、bcl-2及Survivin的mRNA表达来实现的.
目的 研究二甲雙胍在體外對人胰腺癌細胞BxPC 3、AsPC 1生長增殖、凋亡的影響及其抗腫瘤相關分子機製.方法 體外培養人胰腺癌BxPC-3、AsPC 1細胞,四甲基偶氮唑鹽(MTT)法檢測二甲雙胍在不同濃度和不同時間對于胰腺癌細胞增殖的影響,併計算IC50值.用末耑脫氧覈苷痠轉移酶介導的dUTP缺口末耑標記測定(TUNEL)法檢測處理後細胞的凋亡情況.RT-PCR法檢測COX-2、bcl-2、Survivin的錶達影響.結果 MTT法檢測顯示,不同濃度二甲雙胍均可抑製BxPC-3、AsPC-1兩種人胰腺癌細胞增殖,兩種胰腺癌細胞IC50分彆為68.882 mmol/L和90.984 mmol/L.TUNEL法檢測人胰腺癌細胞BxPC-3,正常對照組及二甲雙胍榦預組(以1/2 IC50濃度處理胰腺癌細胞)凋亡率分彆為(2.44±0.57)％和(17.52±0.75)％,P＜0.05；胰腺癌細胞AsPC-1在正常對照組及二甲雙胍榦預組凋亡率分彆為(5.35±0.92)％和(45.76±1.87)％,P＜0.05.RT-PCR結果顯示:人胰腺癌細胞BxPC-3在正常對照組及二甲雙胍榦預組COX-2的mRNA灰度值分彆為0.769±0.006和0.305±0.009,P＜0.05； bcl-2的mRNA灰度值分彆為0.401±0.022和0.129±0.010,P＜0.05；Survivin的mRNA灰度值分彆為0.943±0.029和0.143±0.050,P＜0.05.人胰腺癌AsPC-1細胞在正常對照組及二甲雙胍榦預組COX-2的mRNA灰度值分彆為1.232±0.011和0.831±0.022,P＜0.05；bcl-2的mRNA灰度值分彆為0.400±0.053和0.129±0.032,P＜0.05；Survivin的mRNA灰度值分彆為0.983±0.017和0.174±0.029,P＜0.05.結論 二甲雙胍抑製胰腺癌細胞增殖、促進凋亡.二甲雙胍抗腫瘤機製可能是通過抑製COX-2、bcl-2及Survivin的mRNA錶達來實現的.
목적 연구이갑쌍고재체외대인이선암세포BxPC 3、AsPC 1생장증식、조망적영향급기항종류상관분자궤제.방법 체외배양인이선암BxPC-3、AsPC 1세포,사갑기우담서염(MTT)법검측이갑쌍고재불동농도화불동시간대우이선암세포증식적영향,병계산IC50치.용말단탈양핵감산전이매개도적dUTP결구말단표기측정(TUNEL)법검측처리후세포적조망정황.RT-PCR법검측COX-2、bcl-2、Survivin적표체영향.결과 MTT법검측현시,불동농도이갑쌍고균가억제BxPC-3、AsPC-1량충인이선암세포증식,량충이선암세포IC50분별위68.882 mmol/L화90.984 mmol/L.TUNEL법검측인이선암세포BxPC-3,정상대조조급이갑쌍고간예조(이1/2 IC50농도처리이선암세포)조망솔분별위(2.44±0.57)％화(17.52±0.75)％,P＜0.05；이선암세포AsPC-1재정상대조조급이갑쌍고간예조조망솔분별위(5.35±0.92)％화(45.76±1.87)％,P＜0.05.RT-PCR결과현시:인이선암세포BxPC-3재정상대조조급이갑쌍고간예조COX-2적mRNA회도치분별위0.769±0.006화0.305±0.009,P＜0.05； bcl-2적mRNA회도치분별위0.401±0.022화0.129±0.010,P＜0.05；Survivin적mRNA회도치분별위0.943±0.029화0.143±0.050,P＜0.05.인이선암AsPC-1세포재정상대조조급이갑쌍고간예조COX-2적mRNA회도치분별위1.232±0.011화0.831±0.022,P＜0.05；bcl-2적mRNA회도치분별위0.400±0.053화0.129±0.032,P＜0.05；Survivin적mRNA회도치분별위0.983±0.017화0.174±0.029,P＜0.05.결론 이갑쌍고억제이선암세포증식、촉진조망.이갑쌍고항종류궤제가능시통과억제COX-2、bcl-2급Survivin적mRNA표체래실현적.
Objective Metformin has recently been associated with a decreased risk of pancreatic cancer,but the mechanisms that cause the lower risk are unknown.Therefore,BxPC-3 and AsPc-1 pancreatic cancel cells lines were used to investigate the molecular mechanism and modulating effect of metformin on proliferation and apoptosis.Methods Cells were incubated with metformin in different concentration for 24,48,and 72 hours.Cell viability was then measured and calculated by MTT assay and IC50,respectively,and cell apoptosis was evaluated by TUNEL.Additional,RT-PCR was used to evaluate the expression of COX-2 and Bcl-2 survivin.Results Both BxPC-3 and AsPC-1 cell viability were inhibited by metformin and showed a time-dependent and dose-dependent manner of inhibition effects.The IC50 of the BxPC-3 cell lines were 68.882 mmol/L,24 hours; 64.492 mmol/L,48 hours;and 62.741 mmol/L,72 hours.The IC50 of the AsPC-1 cell lines were 134.372 mmol/L,24 hours;90.984 mmol/L,48 hours; and 61.445 mmol/L,72 hours.TUNEL showed the apoptosis ratios of the BxPC-3 control and metformin group were (2.44±0.57)％ and (17.52±0.75)％.The AsPC-1 ratios were (5.35 ± 0.92) ％ and(45.76 ± 1.87) ％,and both sets of ratios expressed P＜0.05.Also,RT-PCR showed that the expression of COX-2 and Bcl-2 survivin were down-regulated.In BxPC-3,the expressions COX-2 mRNA were 0.769±0.006 and 0.305±0.009,Bcl-2 were 0.401±0.022 and 0.129±0.010,andsurvivin were0.943±0.029 and 0.143±0.050,all with P＜0.05.In AsPC-1,the expressions of COX-2 were 1.232±0.011 and 0.831±0.022,Bcl-2 were 0.400±0.053 and 0.129±0.032,and survivin were 0.983±0.017 and 0.174±0.029,all with P＜0.05.Conclusion Metformin was able to potently inhibit cell growth via regulation of proliferation inhibition and apoptosis induction and therefore inhibited the expression of COX-2,Bcl-2 and survivin preferentially in pancreatic cancer cell lines.
