Self-assembly of cytotoxic peptide conjugated poly(β-amino ester)s for synergistic cancer chemotherapy

J Mater Chem B. 2015 Apr 21;3(15):2943-2953. doi: 10.1039/c4tb02144d. Epub 2015 Mar 11.

Abstract

Nanotechnology has played an important role in cancer therapy due to the potential advantages of nano-drugs including enhanced accumulation in the tumor sites, improved pharmacokinetics and minimized systemic toxicity in vivo. Self-assembled peptides can improve the cellular internalization of peptides effectively through the endocytosis pathway for enhanced bioavailability. Herein, cytotoxic peptide (KLAKLAK)2 (named KLAK) conjugated poly(β-amino ester)s (PAE-KLAK) were synthesized by Michael-type addition. The copolymers could self-assemble into micelle-like nanoparticles with pH-sensitive properties, which were measured by dynamic light scattering (DLS) and transmission electron microscopy (TEM). The endocytosis pathway, mitochondria-regulated apoptosis and enhanced cytotoxicity of P2-KLAK micelles were proved by lysosome colocalization, JC-1 assay and CCK-8 assay in human breast cancer cells (MCF-7 cells), respectively. The cancer cell killing effect of P2-KLAK micelles was higher than that of free KLAK, which could be attributed to the efficient internalization into cells via an endocytosis pathway and a subsequent disruption of mitochondria in cells. Encapsulation of anti-cancer drug doxorubicin (DOX) into P2-KLAK micelles realized the co-delivery of the chemotherapeutic drug and the peptide drug with acid-triggered release in cells. The treatment efficacy of DOX-loaded P2-KLAK micelles was higher than that of DOX-loaded P2 micelles and blank P2-KLAK micelles, indicating their synergistic ability to kill MCF-7 cells. Finally, In vivo tumor imaging and growth inhibition were evaluated in MCF-7 cell-xenografted nude mice, demonstrating that DOX-loaded P2-KLAK micelles could inhibit tumor growth effectively with a one order magnitude lower injection amount of DOX, which was attributed to the specific accumulation in tumor sites, efficient cellular entry and controlled intracellular release of therapeutic drugs.