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首页> 外文期刊>World Journal of Gastroenterology >Effect of caffeicacid phenethyl ester on proliferation and apoptosis of colorectal cancer cells in vitro
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Effect of caffeicacid phenethyl ester on proliferation and apoptosis of colorectal cancer cells in vitro

机译：咖啡酸苯乙酯对结直肠癌细胞体外增殖和凋亡的影响

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摘要

ABM: To study the effect of caffeic acid phenethyl ester (CAPE) on proliferation, cell cycle, apoptosis and expression of β-catenin in cultured human colorectal cancer (CRC) cell line HCT116. METHODS: HCT116 cells were treated with CAPE at serial concentrations of 80, 40, 20, 10, 5, 2.5 mg/L. The proliferative status of HCT116 cells was measured by using methaben-zthiazuron (MTT) assay. Cell cycle was analyzed by using flow cytometry (FCM) with propidium iodide (PI) labeling method. The rate of apoptosis was detected by using FCM with annexin V-FITC and PI double labeling method. β-catenin levels were determined by Western blotting. β-catenin localization in HCT116 was determined by indirect immunofluorescence. RESULTS: After HCT116 cells were exposed to CAPE (80, 40, 20, 10, 5, and 2.5 mg/L) for 24, 48, 72, 96 h, CAPE displayed a strong growth inhibitory effect in a dose- and time-dependent manner against HCT116 cells. FCM analysis showed that the ratio of G_0/G_1 phase cells increased, S phase ratio decreased and apoptosis rate increased after HCT116 cells were exposed to CAPE (10, 5, and 2.5 mg/L) for 24 h. CAPE treatment was associated with decreased cytoplasmic β-catenin, nuclear β-catenin and a concurrent increase in β-catenin protein expression at cell-cell junctions. CONCLUSION: CAPE could inhibit HCT116 cell proliferation and induce cell cycle arrest and apoptosis. Decreased β-catenin protein expression may mediate the anti-proliferative effects of CAPE.
机译：ABM：研究咖啡酸苯乙酯（CAPE）对培养的人结直肠癌（CRC）细胞HCT116增殖，细胞周期，凋亡和β-连环蛋白表达的影响。方法：CAPE以80、40、20、10、5、2.5 mg / L的系列浓度处理HCT116细胞。 HCT116细胞的增殖状态通过使用甲乙ben噻唑啉酮（MTT）测定来测量。通过使用流式细胞术（FCM）和碘化丙啶（PI）标记方法分析细胞周期。 FCM结合膜联蛋白V-FITC和PI双标记法检测细胞凋亡率。 β-连环蛋白水平通过蛋白质印迹法测定。通过间接免疫荧光测定HCT116中的β-catenin定位。结果：HCT116细胞暴露于CAPE（80、40、20、10、5和2.5 mg / L）24、48、72、96 h后，CAPE在剂量和时间上均表现出强大的生长抑制作用。 HCT116细胞的依赖方式。 FCM分析表明，HCT116细胞分别暴露于CAPE（10、5和2.5 mg / L）24 h后，G_0 / G_1期细胞比例增加，S期比例降低，凋亡率增加。 CAPE治疗与细胞质β-catenin减少，核β-catenin减少以及细胞-细胞连接处β-catenin蛋白表达同时增加有关。结论：CAPE可抑制HCT116细胞增殖，诱导细胞周期阻滞和凋亡。 β-catenin蛋白表达降低可能介导CAPE的抗增殖作用。

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