MMP-9 triggered self-assembly of doxorubicin nanofiber depots halts tumor growth

A central challenge in cancer care is to ensure that therapeutic compounds reach their targets. One approach is to use enzyme-responsive biomaterials, which reconfigure in response to endogenous enzymes that are overexpressed in diseased tissues, as potential site-specific anti-tumoral therapies. He...

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Vydáno v:	Biomaterials Ročník 98; s. 192 - 202
Hlavní autoři:	Kalafatovic, Daniela, Nobis, Max, Son, Jiye, Anderson, Kurt I., Ulijn, Rein V.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	Netherlands Elsevier Ltd 01.08.2016
Témata:	Advanced Basic Science animal models Animals biocompatible materials Biomaterials Biomedical materials Cancer therapy Cell Line, Tumor Cell Proliferation - drug effects Dentistry Doxorubicin Doxorubicin - pharmacology Doxorubicin - therapeutic use Drug Carriers - chemistry Enzymes Humans hydrolysis Matrix Metalloproteinase 9 - metabolism Mice, Nude Micelles MMP Morphology transition nanofibers Nanofibers - chemistry Nanofibers - ultrastructure Nanostructure Neoplasm Invasiveness neoplasms Neoplasms - drug therapy Neoplasms - pathology Peptides Peptides - pharmacology Self assembly Surgical implants tissues Tumors MMP Self-assembly Peptides Morphology transition Cancer therapy
ISSN:	0142-9612, 1878-5905, 1878-5905
On-line přístup:	Získat plný text
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Shrnutí:	A central challenge in cancer care is to ensure that therapeutic compounds reach their targets. One approach is to use enzyme-responsive biomaterials, which reconfigure in response to endogenous enzymes that are overexpressed in diseased tissues, as potential site-specific anti-tumoral therapies. Here we report peptide micelles that upon MMP-9 catalyzed hydrolysis reconfigure to form fibrillar nanostructures. These structures slowly release a doxorubicin payload at the site of action. Using both in vitro and in vivo models, we demonstrate that the fibrillar depots are formed at the sites of MMP-9 overexpression giving rise to enhanced efficacy of doxorubicin, resulting in inhibition of tumor growth in an animal model.
Bibliografie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0142-9612 1878-5905 1878-5905
DOI:	10.1016/j.biomaterials.2016.04.039