Zinc oxide nanoparticles (ZnO) are presented as potential cancer therapeutic agent based on their surface properties. In this study, the most abundant blood proteins, albumin, fibrinogen and apo-transferrin, were covalently bound (c-ZnO NPs) and nonspecifically adsorbed (n-ZnO NPs) onto ZnO NPs to evaluate the role of modification route on protein structure and their effects on glioblastoma cells. The success of modification and structures of proteins on ZnO NPs were characterized with FT-IR. It was found that non-covalent interaction significantly damaged the secondary structure of proteins compared to those covalently attached to the ZnO nanoparticle. The effects of modified ZnO NPs were investigated by evaluating viability, cycle, and death mechanisms of glioblastoma (U373) cells. n-ZnO NPs were found more toxic compared to the pristine and c-ZnO NPs. However, c-ZnO NPs with albumin and apo-transferrin both perturbed the cell cycle function, and decreased the necrotic cell death rate of U373 cells below toxic concentration, suggesting their potential curative effect on glioblastoma cells.
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http://dx.doi.org/10.1016/j.ijbiomac.2018.06.059 | DOI Listing |
Discov Oncol
January 2025
Department of Neurosurgery, China-Japan Union Hospital of Jilin University, Changchun, 130033, Jilin, China.
Nucleotide-binding oligomerization domain protein 1 (NOD1) is one of the innate immune receptors that has been associated with tumorigenesis and abnormally expressed in various cancers. However, the role of NOD1 in Glioblastoma Multiforme (GBM) has not been investigated. We used the Tumor Immune Estimate Resource (TIMER) database to compare the differential expression of NOD1 in various tumors.
View Article and Find Full Text PDFSmall
January 2025
Cancer Hospital of Dalian University of Technology, Dalian University of Technology, Shenyang, 110042, China.
Glioblastoma (GBM), the most malignant brain tumor with high prevalence, remains highly resistant to the existing immunotherapies due to the significant immunosuppression within tumor microenvironment (TME), predominantly manipulated by M2-phenotypic tumor-associated macrophages (M2-TAMs). Here in this work, an M2-TAMs targeted nano-reprogrammers, MG5-S-IMDQ, is established by decorating the mannose molecule as the targeting moiety as well as the toll-like receptor (TLR) 7/8 agonist, imidazoquinoline (IMDQ) on the dendrimeric nanoscaffold. MG5-S-IMDQ demonstrated an excellent capacity of penetrating the blood-brain barrier (BBB) as well as selectively targeting M2-TAMs in the GBM microenvironment, leading to a phenotype transformation and function restoration of TAMs shown as heightened phagocytic activity toward tumor cells, enhanced cytotoxic effects, and improved tumor antigen cross-presentation capability.
View Article and Find Full Text PDFCancers (Basel)
December 2024
Hugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA.
: CSCs are critical drivers of the tumor and stem cell phenotypes of glioblastoma (GBM) cells. Chromatin modifications play a fundamental role in driving a GBM CSC phenotype. The goal of this study is to further our understanding of how stem cell-driving events control changes in chromatin architecture that contribute to the tumor-propagating phenotype of GBM.
View Article and Find Full Text PDFCancers (Basel)
December 2024
Research Group on Tumors of the Central Nervous System, Pathology Department, University of Valencia, 46010 Valencia, Spain.
Glioblastoma IDH wild type (GB), the most common malignant primary brain tumor, is characterized by rapid proliferation, extensive infiltration into surrounding brain tissue, and significant resistance to current therapies. Median survival is only 15 months despite extensive clinical efforts. The tumor microenvironment (TME) in GB is highly specialized, supporting the tumor's aggressive behavior and its ability to evade conventional treatments.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Departamento de Biología Molecular y Bioquímica, Universidad de Málaga, 29071 Málaga, Spain.
Glutaminase controls the first step in glutaminolysis, impacting bioenergetics, biosynthesis and oxidative stress. Two isoenzymes exist in humans, GLS and GLS2. GLS is considered prooncogenic and overexpressed in many tumours, while GLS2 may act as prooncogenic or as a tumour suppressor.
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