Smart Nanozymes for Cancer Therapy: The Next Frontier in Oncology.

Nanomaterials that mimic the catalytic activity of natural enzymes in the complex biological environment of the human body are called nanozymes. Recently, nanozyme systems have been reported with diagnostic, imaging, and/or therapeutic capabilities. Smart nanozymes strategically exploit the tumor microenvironment (TME) by the in situ generation of reactive species or by the modulation of the TME itself to result in effective cancer therapy. This topical review focuses on such smart nanozymes for cancer diagnosis, and therapy modalities with enhanced therapeutic effects. The dominant factors that guide the rational design and synthesis of nanozymes for cancer therapy include an understanding of the dynamic TME, structure-activity relationships, surface chemistry for imparting selectivity, and site-specific therapy, and stimulus-responsive modulation of nanozyme activity. This article presents a comprehensive analysis of the subject including the diverse catalytic mechanisms of different types of nanozyme systems, an overview of the TME, cancer diagnosis, and synergistic cancer therapies. The strategic application of nanozymes in cancer treatment can well be a game changer in future oncology. Moreover, recent developments may pave the way for the deployment of nanozyme therapy into other complex healthcare challenges, such as genetic diseases, immune disorders, and ageing.

Surface refined AuQuercetin nanoconjugate stimulates dermal cell migration: possible implication in wound healing.

Refining nutraceutical conjugated metal nanoparticles (NPs) and understanding their interactions with the cellular micro-environment is necessary for their application in nanomedicine. In the present experiment, we studied the effect of quercetin functionalized gold nanoparticles (AuQurNP) on skin fibroblast and keratinocyte cell migration. Spherical shaped AuQurNPs of 47 nm in size were formed due to the interaction of hydroxyl and carbonyl groups of quercetin with Au atoms as revealed by incremental algorithm-based analysis. AuQurNP containing up to 5 µg l-1 of Au with quercetin (5.2 ± 1.6 ng ml-1) was least toxic to fibroblasts. AuQurNP effectively reduced the generation of intracellular ROS (up to 63%) through free-radical scavenging activity. AuQurNP also enhanced the rate of migration of fibroblasts (24 h) and keratinocytes (20 h) in artificially created wounds. The rate of migration of the cells towards the wound edge was in the order of AuQurNP > control > quercetin > AuNP. AuQurNP also significantly increased the expression of TGFß1 protein, thereby inducing the downstream SMAD complex (SMAD 2-4). Downregulation of the inhibitory protein SMAD 7 by AuQurNP helped in the nuclear translocation of SMADs 3 and 4. Collectively, the present in vitro study demonstrates the action of AuQurNP on the SMAD family and the interconnected molecular mechanism leading to the cell migration process.