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Caffeic Acid Phenethyl Ester Causes p21Cip1 Induction, Akt Signaling Reduction, and Growth Inhibition in PC-3 Human Prostate Cancer Cells

机译:咖啡酸苯乙基酯在PC-3人前列腺癌细胞中引起p21Cip1诱导,Akt信号传导减少和生长抑制

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摘要

Caffeic acid phenethyl ester (CAPE) treatment suppressed proliferation, colony formation, and cell cycle progression in PC-3 human prostate cancer cells. CAPE decreased protein expression of cyclin D1, cyclin E, SKP2, c-Myc, Akt1, Akt2, Akt3, total Akt, mTOR, Bcl-2, Rb, as well as phosphorylation of Rb, ERK1/2, Akt, mTOR, GSK3α, GSK3β, PDK1; but increased protein expression of KLF6 and p21Cip1. Microarray analysis indicated that pathways involved in cellular movement, cell death, proliferation, and cell cycle were affected by CAPE. Co-treatment of CAPE with chemotherapeutic drugs vinblastine, paclitaxol, and estramustine indicated synergistic suppression effect. CAPE administration may serve as a potential adjuvant therapy for prostate cancer.
机译:咖啡酸苯乙酯(CAPE)处理可抑制PC-3人前列腺癌细胞的增殖,集落形成和细胞周期进程。 CAPE降低了细胞周期蛋白D1,细胞周期蛋白E,SKP2,c-Myc,Akt1,Akt2,Akt3,总Akt,mTOR,Bcl-2,Rb的蛋白表达以及Rb,ERK1 / 2,Akt,mTOR,GSK3α的磷酸化,GSK3β,PDK1;但增加了KLF6和p21Cip1的蛋白质表达。微阵列分析表明CAPE影响了细胞运动,细胞死亡,增殖和细胞周期的相关途径。 CAPE与化学治疗药物长春碱,紫杉醇和雌莫司汀的共同治疗显示协同抑制作用。 CAPE的给药可以作为前列腺癌的潜在辅助疗法。

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