Nanoconjugation: A Materials Approach to Enhance Epidermal Growth Factor Induced Apoptosis.
Nanoconjugation: A Materials Approach to Enhance Epidermal Growth Factor Induced Apoptosis.
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DOI：
10.1039/c3bm60142k
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发表时间：
2014-02-01
影响因子：
6.6
通讯作者：
Reinhard BM
中科院分区：
文献类型：
--
作者：
Wu L;Yu X;Feizpour A;Reinhard BM
细胞凋亡逃避是癌症的一个标志，这促使人们开发出以受控方式诱导细胞死亡的新策略。纳米颗粒(NPs)与细胞成分的大小相容为调控细胞过程提供了新的机会，可能包括细胞凋亡。我们研究了表皮生长因子(EGF)共价连接到直径40 nm的Au纳米颗粒对两种体外癌细胞株A431和HeLa细胞凋亡水平的影响，以caspase-3活性表示。我们的研究表明，纳米偶联增强了EGF诱导过表达A431的EGF受体(EGFR)的凋亡，并触发了HeLa中可量化的凋亡增加。后者有生理性受体表达水平，不显示对游离EGF的凋亡反应。内吞作用和运输参与了关键的EGFR调节过程，最重要的是信号终止。我们的实验结果表明，这些过程可以通过纳米连接来诱导细胞凋亡。
Apoptosis evasion is a hallmark of cancer that motivates the development of novel strategies for inducing cell death in a controlled fashion. The size-compatibility of nanoparticles (NPs) with cellular components provides new opportunities for regulating cellular processes, potentially including apoptosis. We investigated the impact of the covalent attachment of epidermal growth factor (EGF) to 40 nm diameter Au NPs on cellular apoptosis levels, quantified as caspase-3 activity, in two in vitro cancer cell lines: A431 and HeLa. Our studies show that nanoconjugation enhances EGF-induced apoptosis in EGF receptor (EGFR) overexpressing A431 and triggers a quantifiable increase in apoptosis in HeLa. The latter has physiological receptor expression levels and does not show apoptosis in response to free EGF. Endocytosis and trafficking are involved in key EGFR regulation processes, most prominently signal termination. Our experimental findings indicate that these processes can be manipulated through nanoconjugation to induce apoptosis.