In situ generated D-peptidic nanofibrils as multifaceted apoptotic inducers to target cancer cells

被引:46
作者
Du, Xuewen [1 ]
Zhou, Jie [1 ]
Wang, Huainin [1 ]
Shi, Junfeng [1 ]
Kuang, Yi [1 ]
Zeng, Wu [2 ]
Yang, Zhimou [3 ]
Xu, Bing [1 ]
机构
[1] Brandeis Univ, Dept Chem, 415 South St, Waltham, MA 02454 USA
[2] Brandeis Univ, Heller Sch Social Policy & Management, Waltham, MA 02454 USA
[3] Nankai Univ, Coll Life Sci, Tianjin 300071, Peoples R China
来源
CELL DEATH & DISEASE | 2017年 / 8卷
关键词
TUMOR-NECROSIS-FACTOR; PROTEIN-TYROSINE PHOSPHATASES; FACTOR TNF RECEPTOR; ALKALINE-PHOSPHATASE; ENZYMATIC FORMATION; FACTOR-ALPHA; DEATH; VIVO; PROLIFERATION; CYTOTOXICITY;
D O I
10.1038/cddis.2016.466
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Nanofibrils of small molecules, as a new class of biofunctional entities, exhibit emergent properties for controlling cell fates, but the relevant mechanism remains to be elucidated and the in vivo effect has yet to be examined. Here, we show that D-peptide nanofibrils, generated by enzyme-instructed self-assembly (EISA), pleiotropically activate extrinsic death signaling for selectively killing cancer cells. Catalyzed by alkaline phosphatases and formed in situ on cancer cells, D-peptide nanofibrils present autocrine proapoptotic ligands to their cognate receptors in a juxtacrine manner, as well as directly cluster the death receptors. As multifaceted initiators, D-peptide nanofibrils induce apoptosis of cancer cells without harming normal cells in a co-culture, kill multidrug-resistant (MDR) cancer cells, boost the activities of anticancer drugs, and inhibit tumor growth in a murine model. Such a supramolecular cellular biochemical process (consisting of reaction, assembly, and binding) for multi-targeting or modulating protein-protein interaction networks ultimately may lead to new ways for combating cancer drug resistance.
引用
收藏
页码:e2614 / e2614
页数:11
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