胃肠病学
胃腸病學
위장병학
CHINESE JOURNAL OF GASTROENTEROLOGY
2014年
11期
650-654
,共5页
慕刚刚%于红刚%李红艳%李维
慕剛剛%于紅剛%李紅豔%李維
모강강%우홍강%리홍염%리유
胰腺肿瘤%百里醌%肿瘤转移%肿瘤侵润%黏着斑激酶
胰腺腫瘤%百裏醌%腫瘤轉移%腫瘤侵潤%黏著斑激酶
이선종류%백리곤%종류전이%종류침윤%점착반격매
Pancreatic NeopIasms%Thymoquinone%Tumor Metastasis%NeopIasm Invasiveness%FocaI Adhesion Kinase
背景：胰腺癌是恶性程度最高的消化道肿瘤，目前吉西他滨依赖的化疗对抑制胰腺癌转移的治疗效果欠佳。研究发现百里醌对多种肿瘤细胞具有抑制增殖、促进凋亡的作用。目的：探讨百里醌对人胰腺癌BxPC-3细胞体外运动和侵袭的影响及其作用机制。方法：常规培养人胰腺癌细胞株BxPC-3，加入不同浓度百里醌进行处理。采用Boyden小室法检测细胞体外运动、侵袭情况；蛋白质印迹法检测细胞FAK、Akt蛋白表达和Akt磷酸化水平的改变；免疫荧光技术检测细胞内FAK表达、细胞黏着斑和F-actin的变化。结果：10、25μmoI/L百里醌对BxPC-3细胞体外运动的抑制率分别为43.4%、73.8%，对体外侵袭的抑制率分别为60.5%、75.6%，百里醌呈浓度依赖性地抑制胰腺癌BxPC-3细胞的体外运动、侵袭（P＜0.05）。百里醌能明显下调BxPC-3细胞FAK表达，并抑制细胞磷酸化Akt的激活。百里醌可诱导FAK弥散分布于胞质，明显抑制黏着斑形成和F-actin的聚合集化。结论：百里醌通过抑制FAK/PI3K/Akt通路的信号转导和激酶活性，浓度依赖性地抑制人胰腺癌BxPC-3细胞的体外运动和侵袭。
揹景：胰腺癌是噁性程度最高的消化道腫瘤，目前吉西他濱依賴的化療對抑製胰腺癌轉移的治療效果欠佳。研究髮現百裏醌對多種腫瘤細胞具有抑製增殖、促進凋亡的作用。目的：探討百裏醌對人胰腺癌BxPC-3細胞體外運動和侵襲的影響及其作用機製。方法：常規培養人胰腺癌細胞株BxPC-3，加入不同濃度百裏醌進行處理。採用Boyden小室法檢測細胞體外運動、侵襲情況；蛋白質印跡法檢測細胞FAK、Akt蛋白錶達和Akt燐痠化水平的改變；免疫熒光技術檢測細胞內FAK錶達、細胞黏著斑和F-actin的變化。結果：10、25μmoI/L百裏醌對BxPC-3細胞體外運動的抑製率分彆為43.4%、73.8%，對體外侵襲的抑製率分彆為60.5%、75.6%，百裏醌呈濃度依賴性地抑製胰腺癌BxPC-3細胞的體外運動、侵襲（P＜0.05）。百裏醌能明顯下調BxPC-3細胞FAK錶達，併抑製細胞燐痠化Akt的激活。百裏醌可誘導FAK瀰散分佈于胞質，明顯抑製黏著斑形成和F-actin的聚閤集化。結論：百裏醌通過抑製FAK/PI3K/Akt通路的信號轉導和激酶活性，濃度依賴性地抑製人胰腺癌BxPC-3細胞的體外運動和侵襲。
배경：이선암시악성정도최고적소화도종류，목전길서타빈의뢰적화료대억제이선암전이적치료효과흠가。연구발현백리곤대다충종류세포구유억제증식、촉진조망적작용。목적：탐토백리곤대인이선암BxPC-3세포체외운동화침습적영향급기작용궤제。방법：상규배양인이선암세포주BxPC-3，가입불동농도백리곤진행처리。채용Boyden소실법검측세포체외운동、침습정황；단백질인적법검측세포FAK、Akt단백표체화Akt린산화수평적개변；면역형광기술검측세포내FAK표체、세포점착반화F-actin적변화。결과：10、25μmoI/L백리곤대BxPC-3세포체외운동적억제솔분별위43.4%、73.8%，대체외침습적억제솔분별위60.5%、75.6%，백리곤정농도의뢰성지억제이선암BxPC-3세포적체외운동、침습（P＜0.05）。백리곤능명현하조BxPC-3세포FAK표체，병억제세포린산화Akt적격활。백리곤가유도FAK미산분포우포질，명현억제점착반형성화F-actin적취합집화。결론：백리곤통과억제FAK/PI3K/Akt통로적신호전도화격매활성，농도의뢰성지억제인이선암BxPC-3세포적체외운동화침습。
BacKground:Human pancreatic cancer is a highIy maIignant tumor of digestive system. CurrentIy,gemcitabine based conventionaI chemotherapy has onIy very Iimited efficacy on metastasis of pancreatic cancer. Studies have shown that thymoquinone has remarkabIe effect of inhibiting proIiferation and enhancing apoptosis on a variety of cancer ceIIs. Aims:To investigate the effect and mechanism of thymoquinone on inhibiting the migration and invasion of human pancreatic cancer BxPC-3 ceIIs in vitro. Methods:Human pancreatic cancer BxPC-3 ceIIs were conventionaIIy cuItured and treated with different concentrations of thymoquinone. The migration and invasion of BxPC-3 ceIIs were determined by Boyden chamber assay. The expressions of FAK,Akt and phosphoryIation of Akt were measured by Western bIotting,and immunofIuorescence was used to detect expression of FAK,focaI adhesions and F-actin. Results:The inhibitory rates of 10,25μmoI/L thymoquinone on migration of BxPC-3 ceIIs were 43. 4% and 73. 8%,respectiveIy,and the inhibitory rates of invasion were 60. 5% and 75. 6%,respectiveIy. The reduction of migration and invasion of pancreatic cancer BxPC-3 ceIIs by thymoquinone was in a dose-dependent manner( P < 0. 05 ). Thymoquinone obviousIy down-reguIated the expression of FAK and suppressed the phosphoryIation of Akt in BxPC-3 ceIIs. Thymoquinone induced the dispersed distribution of FAK in cytopIasm and inhibited the formation of focaI adhesions and assembIy of F-actin. Conclusions:Thymoquinone inhibits the migration and invasion of human pancreatic cancer BxPC-3 ceIIs in a dose-dependent manner in vitro through suppression of FAK/PI3K/Akt signaIing pathway and activity of kinase.
