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从构巢曲霉中提取的asperfuranone 通过阻断细胞周期进程和诱导细胞凋亡来抑制人非小细胞肺癌 A549 细胞的增殖。

Asperfuranone from Aspergillus nidulans inhibits proliferation of human non-small cell lung cancer A549 cells via blocking cell cycle progression and inducing apoptosis.

机构信息

Department of Pharmacology and Pharmaceutical Science, University of Southern California, School of Pharmacy, Los Angeles, CA, USA.

出版信息

Basic Clin Pharmacol Toxicol. 2010 Jul;107(1):583-9. doi: 10.1111/j.1742-7843.2010.00545.x. Epub 2010 Feb 9.

Abstract

Asperfuranone, a novel compound of genomic mining in Aspergillus nidulans, was investigated for its anti-proliferative activity in human non-small cell lung cancer A549 cells. To identity the anti-cancer mechanism of asperfuranone, we assayed its effect on apoptosis, cell cycle distribution, and levels of p53, p21 Waf1/Cip1, Fas/APO-1 receptor and Fas ligand. Enzyme-linked immunosorbent assay showed that the G0/G1 phase arrest might be due to p53-dependent induction of p21 Waf1/Cip1. An enhancement in Fas/APO-1 and its two form ligands, membrane-bound Fas ligand (mFasL) and soluble Fas ligand (sFasL), might be responsible for the apoptotic effect induced by asperfuranone. Our study reports here for the first time that the induction of p53 and the activity of Fas/Fas ligand apoptotic system may participate in the anti-proliferative activity of asperfuranone in A549 cells.

摘要

作为从构巢曲霉中基因组挖掘得到的一种新型化合物,asperfuranone 被研究其在人类非小细胞肺癌 A549 细胞中的抗增殖活性。为了确定 asperfuranone 的抗癌机制,我们检测了它对细胞凋亡、细胞周期分布以及 p53、p21 Waf1/Cip1、Fas/APO-1 受体和 Fas 配体水平的影响。酶联免疫吸附试验表明,G0/G1 期阻滞可能是由于 p53 依赖性诱导 p21 Waf1/Cip1。Fas/APO-1 及其两种形式的配体,膜结合 Fas 配体 (mFasL) 和可溶性 Fas 配体 (sFasL) 的增强可能是 asperfuranone 诱导凋亡的原因。我们的研究首次报道,p53 的诱导和 Fas/Fas 配体凋亡系统的活性可能参与了 asperfuranone 在 A549 细胞中的抗增殖活性。

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