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阿魏酸苯乙酯可诱导 PC-3 人前列腺癌细胞中 p21 的表达,降低 Akt 信号转导,并抑制其生长。

Caffeic acid phenethyl ester causes p21 induction, Akt signaling reduction, and growth inhibition in PC-3 human prostate cancer cells.

机构信息

Institute of Cellular and System Medicine, National Health Research Institutes, Miaoli, Taiwan.

出版信息

PLoS One. 2012;7(2):e31286. doi: 10.1371/journal.pone.0031286. Epub 2012 Feb 7.

Abstract

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 p21(Cip1). 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.

摘要

咖啡酸苯乙酯(CAPE)处理抑制了 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、E、SKP2、c-Myc、Akt1、Akt2、Akt3、总 Akt、mTOR、Bcl-2、Rb 以及 Rb、ERK1/2、Akt、mTOR、GSK3α、GSK3β、PDK1 的磷酸化蛋白的表达;但增加了 KLF6 和 p21(Cip1)的蛋白表达。微阵列分析表明,细胞运动、细胞死亡、增殖和细胞周期相关的途径受到 CAPE 的影响。CAPE 与化疗药物长春碱、紫杉醇和雌莫司汀联合治疗表明具有协同抑制作用。CAPE 的给药可能作为前列腺癌的一种潜在辅助治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6191/3274546/564b53fa1971/pone.0031286.g001.jpg

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