RESUMO
Ferroptosis, first suggested in 2012, is a type of non-apoptotic programmed cell death caused by the buildup of lipid peroxidation and marked by an overabundance of oxidized poly unsaturated fatty acids. During the last decade, researchers have uncovered the formation of ferroptosis and created multiple drugs aimed at it, but due to poor selectivity and pharmacokinetics, clinical application has been hindered. In recent years, biomedical discoveries and developments in nanotechnology have spurred the investigation of ferroptosis nanomaterials, providing new opportunities for the ferroptosis driven tumours treatment. Additionally, hydrogels have been widely studied in ferroptosis because of their unique 3D structure and excellent controllability. By using these biomaterials, it is possible to achieve controlled release and targeted delivery of drugs, thus increasing the potency of the drugs and minimizing adverse effects. Therefore, summarizing the biomedical nanomaterials, including hydrogels, used in ferroptosis for cancer therapy is a must. This article provides an overview of ferroptosis, detailing its properties and underlying mechanisms. It also categorizes and reviews the use of various nanomaterials in ferroptosis, along with relevant explanations and illustrations. In addition, we discuss the opportunities and challenges facing the application of nanomaterials in ferroptosis. Finally, the development prospects of this field are prospected. This review is intended to provide a foundation for the development and application of biomedical nanomaterials in ferroptosis.
Assuntos
Ferroptose , Nanoestruturas , Neoplasias , Materiais Biocompatíveis/farmacologia , Materiais Biocompatíveis/uso terapêutico , Hidrogéis , Nanotecnologia , Neoplasias/tratamento farmacológicoRESUMO
In order to improve the delivery efficiency of microRNA (miRNA or miR)-145, the present study examined several factors which may affect cationic liposome (CL)-based transfection, including the hydration medium used for the preparation of liposomes, the quantity of the plasmid, the molar ratio of N-[1-(2,3-dioleoyloxy)propyl]-N,N,N-trimethylammonium chloride (DOTAP)/cholesterol (chol), or DOTAP/chol, and the weight ratio of DOTAP/DNA. In order to enhance the transfection efficiency, protamine was selected as a DNA-condensing agent to form liposomeprotamineDNA (LPD) ternary complexes. An agarose gel retardation assay was used to examine the DNA binding affinity of the CLs. Following transfection, GFP fluorescence images were captured and flow cytometry was performed to determine the transfection efficiency. Furthermore, an MTT assay was performed to determine the cytotoxicity of the liposome complexes. The final optimal conditions were as follows: 5% glucose as the hydration medium, a molar ratio of DOTAP/chol at 3:1 for the preparation of CLs, a weight ratio of DOTAP/protamine/DNA of 3:0.5:1, with 8 µg plasmid added for the preparation of the LPD complexes. In vitro, the LPD complexes exhibited an enhanced transfection efficiency and low cytotoxicity, which indicated that the presented LPD vector enhanced the transfection efficiency of the CLs. The HepG2 cells were found to have the lowest expression levels of miR145 out of the cell lines tested (A549, BGC-823, HepG2, HeLa, LoVo and MCF-7). Following the transient transfection of the HepG2 cells with miR145, the results revealed that the overexpression of miR145 inhibited the proliferation of the HepG2 cells and downregulated the expression of cyclin-dependent kinase 6 (CDK6), cyclinD1, c-myc, and Sp1 transcription factor (Sp1). In conclusion, in this study, we optimized a liposomebased delivery system for the efficient delivery of miR145 into cancer cells. This may provide a foundation for further research into the use of miR145 in anticancer therapeutics.