Innovative Applications of Plant Viruses in Drug Targeting and Molecular Imaging- A review.

BackgroundNature had already engineered various types of nanoparticles (NPs), especially viruses, which can deliver their cargo to the host/targeted cells. The ability to selectively target specific cells offers a significant advantage over the conventional approach. Numerous organic NPs, including native protein cages, virus-like pieces, polymeric saccharides, and liposomes, have been used for the preparation of nanoparticulate. Such nanomaterials have demonstrated better performance and as well as improved biocompatible, devoid of side effects, and stable without any deterioration.ObjectiveThis review discusses current clinical and scientific research on naturally occurring nanomaterials. The review illustrates and updates the tailor-made approaches for selective delivery and targeted medications that require a highaffinity interconnection to the targeted cells.MethodA comprehensive search was performed using keywords for viral nanoparticles, viral particles for drug delivery, viral nanoparticles for molecular imaging, theranostics applications of viral nanoparticles and plant viruses in nanomedicine. We searched in Google Scholar, PubMed, Springer, Medline, and Elsevier from 2000 to till date and by the bibliographic review of all identified articles.ResultsThe findings demonstrated that structures dependent on nanomaterials might have potential applications in diagnostics, cell marking, comparing agents (computed tomography and magnetic resonance imaging), and antimicrobial drugs, as well as drug delivery structures. However, measures should be taken in order to prevent or mitigate in pharmaceutical or medical applications the toxic impact or incompatibility of nanoparticle-based structures with biological systems.ConclusionThe review provided an overview of the latest advances in nanotechnology, outlining the difficulties and the advantages of in vivo and in vitro structures that are focused on a specific subset of the natural nanomaterials

A potential MRI agent and an anticancer drug encapsulated within CPMV virus-like particles.

Background: Virus nanoparticles have been extensively studied over the past decades for theranostics applications. Viruses are well-characterized, naturally occurring nanoparticles that can be produced in high quantity with a high degree of similarity in both structure and composition. Objectives: The plant virus Cowpea Mosaic Virus (CPMV) has been innovatively used as a nanoscaffold. Utilization of the internal cavity of empty Virus-Like Particles (VLPs) for the inclusion of therapeutics within the capsid has opened many opportunities in drug delivery and imaging applications. Methods: The encapsidation of magnetic materials and anticancer drugs was achieved. SuperscriptCPMV denotes molecules attached to the external surface of CPMV and CPMVSubscript denotes molecules within the interior of the capsid. Results: Here, the generation of novel VLPs incorporating iron-platinum nanoparticles TCPMVFePt and cisplatin (Cis) (TCPMVCis) is reported. TCPMVCis exhibited a cytotoxic IC50 of TCPMVCis on both A549 and MDA-MB-231 cell lines of 1.8 μM and 3.9 μM, respectively after 72 hours of incubation. The TCPMVFePt were prepared as potential MRI contrast agents. Conclusion: Cisplatin loaded VLP (TCPMVCis) is shown to enhance cisplatin cytotoxicity in cancer cell lines with its potency increased by 2.3-folds

Cigarette smoke metabolically promotes cancer, via autophagy and premature aging in the host stromal microenvironment.

Cigarette smoke has been directly implicated in the disease pathogenesis of a plethora of different human cancer subtypes, including breast cancers. The prevailing view is that cigarette smoke acts as a mutagen and DNA damaging agent in normal epithelial cells, driving tumor initiation. However, its potential negative metabolic effects on the normal stromal microenvironment have been largely ignored. Here, we propose a new mechanism by which carcinogen-rich cigarette smoke may promote cancer growth, by metabolically "fertilizing" the host microenvironment. More specifically, we show that cigarette smoke exposure is indeed sufficient to drive the onset of the cancer-associated fibroblast phenotype via the induction of DNA damage, autophagy and mitophagy in the tumor stroma. In turn, cigarette smoke exposure induces premature aging and mitochondrial dysfunction in stromal fibroblasts, leading to the secretion of high-energy mitochondrial fuels, such as L-lactate and ketone bodies. Hence, cigarette smoke induces catabolism in the local microenvironment, directly fueling oxidative mitochondrial metabolism (OXPHOS) in neighboring epithelial cancer cells, actively promoting anabolic tumor growth. Remarkably, these autophagic-senescent fibroblasts increased breast cancer tumor growth in vivo by up to 4-fold. Importantly, we show that cigarette smoke-induced metabolic reprogramming of the fibroblastic stroma occurs independently of tumor neo-angiogenesis. We discuss the possible implications of our current findings for the prevention of aging-associated human diseases and, especially, common epithelial cancers, as we show that cigarette smoke can systemically accelerate aging in the host microenvironment. Finally, our current findings are consistent with the idea that cigarette smoke induces the "reverse Warburg effect," thereby fueling "two-compartment tumor metabolism" and oxidative mitochondrial metabolism in epithelial cancer cells. KEYWORDS: autophagy, breast cancer, cancer prevention, carcinogens, cigarette smoke, ketone bodies, lactate, microenvironment, mitochondrial dysfunction, premature aging, senescence, tumor growt

The IA-2 interactome

Islet antigen-2 (IA-2), a major autoantigen in type 1 diabetes, is an enzymatically inactive member of the transmembrane protein tyrosine phosphatase (PTP) family. IA-2 is located in dense-core secretory vesicles and is involved in the regulation of insulin secretion. The present experiments were initiated to identify those proteins that interact with IA-2 (i.e. the IA-2 interactome) as a first step towards elucidating the mechanism(s) by which IA-2 influences insulin secretion and serves as an autoantigen.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46036/1/125_2005_Article_37.pd