Advances in Nanomaterials-Based Carrier System for the Treatment of Breast Cancer

Nanotherapeutics for the cure of breast cancer remains unswervingly succeeding and being practiced to eradicate innumerable restrictions of conventional practice obtainable for the supervision of breast cancer. Nanoparticles offer an interdisciplinary extent for exploration in imaging, diagnosis and targeting of breast cancer. Through a progressive physicochemical features and improved bioavailability, they spectacle persistent blood circulation through effective tumor targeting. Nanoparticles remain capable to diminish cytotoxic consequence of the active anticancer medications through amassed cancer cell targeting in contrast to conventional preparations. Several nanoparticles-based preparations remain in the preclinical and clinical phases of progress; amongst them, polymeric drug micelles, liposomes, and dendrimer, remain the utmost common. In this review, we have conferred the role of nanoparticles through detail to oncology, by predominantly aiming on the breast cancer and several nanodelivery systems practiced for targeting action and signaling forces through further intracellular pathways in breast cancer.

Construction of Novel Nanocomposites (Cu-MOF/GOD@HA) for Chemodynamic Therapy

The emerging chemodynamic therapy (CDT) has received an extensive attention in recent years. However, the efficiency of CDT is influenced due to the limitation of H2O2 in tumor. In this study, we designed and synthesized a novel core-shell nanostructure, Cu-metal organic framework (Cu-MOF)/glucose oxidase (GOD)@hyaluronic acid (HA) (Cu-MOF/GOD@HA) for the purpose of improving CDT efficacy by increasing H2O2 concentration and cancer cell targeting. In this design, Cu-MOF act as a CDT agent and GOD carrier. Cu(II) in Cu-MOF are reduced to Cu(I) by GSH to obtain Cu(I)-MOF while GSH is depleted. The depletion of GSH reinforces the concentration of H2O2 in tumor to improve the efficiency of CDT. The resultant Cu(I)-MOF catalyze H2O2 to generate hydroxyl radicals (·OH) for CDT. GOD can catalyze glucose (Glu) to supply H2O2 for CDT enhancement. HA act as a targeting molecule to improve the targeting ability of Cu-MOF/GOD@HA to the tumor cells. In addition, after loading with GOD and coating with HA, the proportion of Cu(I) in Cu-MOF/GOD@HA is increased compared with the proportion of Cu(I) in Cu-MOF. This phenomenon may shorten the reactive time from Cu-MOF to Cu(I)-MOF. The CDT enhancement as a result of GOD and HA effects in Cu-MOF/GOD@HA was evidenced by in vitro cell and in vivo animal studies.

Biocompatible nucleus-targeted graphene quantum dots for selective killing of cancer cells via DNA damage

Graphene quantum dots (GQDs) are nano-sized graphene slices. With their small size, lamellar and aromatic-ring structure, GQDs tend to enter into the cell nucleus and interfere with DNA activity. Thus, GQD alone is expected to be an anticancer reagent. Herein, we developed GQDs that suppress the growth of tumor by selectively damaging the DNA of cancer cells. The amine-functionalized GQDs were modified with nucleus targeting TAT peptides (TAT-NGs) and further grafted with cancer-cell-targeting folic acid (FA) modified PEG via disulfide linkage (FAPEG-TNGs). The resulting FAPEG-TNGs exhibited good biocompatibility, nucleus uptake, and cancer cell targeting. They adsorb on DNA via the π–π and electrostatic interactions, which induce the DNA damage, the upregulation of the cell apoptosis related proteins, and the suppression of cancer cell growth, ultimately. This work presents a rational design of GQDs that induce the DNA damage to realize high therapeutic performance, leading to a distinct chemotherapy strategy for targeted tumor therapy.

Gold nanoparticles conjugated with anti-CD133 monoclonal antibody and 5-fluorouracil chemotherapeutic agent as nanocarriers for cancer cell targeting

5-FU-PEGylated AuNPs-CD133 is designed to improve specific targeting of 5-FU against colorectal cancer cells which abundantly express CD133.

Enhancing the biological activity of polyoxometalate–peptide nano-fibrils by spacer design

The introduction of a tailored hydrophilic/anionic spacer in an Anderson–Evans polyoxometalate, bis-conjugated with demobensin-1 peptide, fosters self-assembly into fibrillary nanostructures and an unprecedented cancer cell targeting ability.

Multi-functional DNA-conjugated nanohydrogels for aptamer-directed breast cancer cell targeting

The development of new conjugation chemistry involving DNA and nanoparticles as well as nanoparticle-based platforms for aptamer-directed cancer-cell targeting is important for improved targeted therapy and imaging. Herein, a dual...

Gramicidin A-based unimolecular channel: cancer cell-targeting behavior and ion transport-induced apoptosis

A series of glycoside-peptide conjugates were prepared by engineering at the N-terminus of natural peptide gramicidin A. The conjugate containing galactose moiety formed unimolecular transmembrane channel and mediated ion transport...

Oncolytic Coxsackievirus and the Mechanisms of its Effects on Cancer: A Narrative Review

Abstract:: Cancer is a genetic disease triggered by gene mutations, which control cell growth and their functionality inherited from previous generations. The targeted therapy of some tumors was not especially successful. A host of new techniques can be used to treat aptamer-mediated targeting, cancer immunotherapy, cancer stem cell (CSC) therapy, cell-penetrating peptides (CPPs), hormone therapy, intracellular cancer cell targeting, nanoparticles, and viral therapy. These include chemical-analog conjugation, gene delivery, ligand-receptor-based targeting, prodrug therapies, and triggered release strategies. Virotherapy is a biotechnological technique for turning viruses into therapeutic agents by the reprogramming of viruses to cure diseases. In several tumors, including melanoma, multiple myeloma, bladder cancer, and breast cancer, the oncolytic capacity of oncolytic Coxsackievirus has been studied. The present study aims to assess oncolytic Coxsackievirus and its mechanisms of effect on cancer cells.