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	Polymer-klak peptide conjugates induce cancer cell death through synergistic effects of mitochondria damage and autophagy blockage
	Qiao, Zeng-Ying1; Lai, Wen-Jia1,2; Lin, Yao-Xin1,3; Li, Dan1,3; Nan, Xiao-Hui1,3; Wang, Yi1,3; Wang, Hao1; Fang, Qiao-Jun1,2,3
刊名	Bioconjugate chemistry
	2017-06-01
卷号	28期号:6页码:1709-1721
ISSN号	1043-1802
DOI	10.1021/acs.bioconjchem.7b00176
通讯作者	Wang, hao(wanghao@nanoctr.cn) ; Fang, qiao-jun(fangqj@nanoctr.cn)
英文摘要	Nanoscaled polymer peptide conjugates (ppcs) containing both functional peptides and synthetic polymer comprise a new family of biomaterials that can circumvent the limitation of peptides alone. our previous work showed that ppcs with the therapeutic peptide klak, especially ppcs with shorter peg spacers and a higher degree of polymerization, exhibit enhanced antitumor effects through disrupting mitochondrial membranes. however, as ppcs have a spherical nanostructure (45-60 nm), this may have other effects besides the conjugated therapeutic peptide klak itself when they enter cancer cells. in this research, we compared the proteome differences of u87 cells treated with klak, polymer, and their conjugates (p-klak) through quantitative proteomics technology. the result reveals that proteins involved in oxidative stress response and the nrf2/are pathway were significantly up regulated after p-klak treatment. moreover, the overexpression of sequestosome 1, a protein substrate that is selectively incorporated into the formation of autophagosome and degraded by autophagy, is found in our study and has not been reported previously in the study of klak toxicity. additional experiments suggest that upon endocytosis, p-klak causes lysosome impairment and results in autophagosomes accumulation. hence, p-klak might induce u87 cell death by autophagy blockage due to lysosome impairment as well as mitochondria damage synergistically.
WOS关键词	SILVER NANOPARTICLES ; SILICA NANOPARTICLES ; TRANSCRIPTION FACTOR ; LYSOSOME IMPAIRMENT ; ANTICANCER ACTIVITY ; PATHWAY MECHANISMS ; SIGNALING PATHWAY ; OXIDATIVE STRESS ; BREAST-CANCER ; SULFINIC ACID
WOS研究方向	Biochemistry & Molecular Biology ; Chemistry
WOS类目	Biochemical Research Methods ; Biochemistry & Molecular Biology ; Chemistry, Multidisciplinary ; Chemistry, Organic
语种	英语
出版者	AMER CHEMICAL SOC
WOS记录号	WOS:000404090500014
内容类型	期刊论文
URI标识	http://www.corc.org.cn/handle/1471x/2177336
专题	高能物理研究所
通讯作者	Wang, Hao; Fang, Qiao-Jun
作者单位	1.Chinese Acad Sci, CAS Ctr Excellence Nanosci, Key Lab Biol Effects Nanomat & Nanosafety, Beijing 100190, Peoples R China 2.Natl Ctr Nanosci & Technol, Beijing Key Lab Ambient Particles Hlth Effects &, Beijing 100190, Peoples R China 3.Univ Chinese Acad Sci, Beijing 100049, Peoples R China
推荐引用方式 GB/T 7714	Qiao, Zeng-Ying,Lai, Wen-Jia,Lin, Yao-Xin,et al. Polymer-klak peptide conjugates induce cancer cell death through synergistic effects of mitochondria damage and autophagy blockage[J]. Bioconjugate chemistry,2017,28(6):1709-1721.
APA	Qiao, Zeng-Ying.,Lai, Wen-Jia.,Lin, Yao-Xin.,Li, Dan.,Nan, Xiao-Hui.,...&Fang, Qiao-Jun.(2017).Polymer-klak peptide conjugates induce cancer cell death through synergistic effects of mitochondria damage and autophagy blockage.Bioconjugate chemistry,28(6),1709-1721.
MLA	Qiao, Zeng-Ying,et al."Polymer-klak peptide conjugates induce cancer cell death through synergistic effects of mitochondria damage and autophagy blockage".Bioconjugate chemistry 28.6(2017):1709-1721.

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