Assessing antioxidant responses in C6 and U-87 MG cell lines exposed to high copper levels.

Copper excess has been tested as an anticancer therapy, due to its properties to generate oxidative stress resulting in tumoral cell death. Thus, this study aimed to evaluate the impact of copper excess on oxidative stress and antioxidant responses in glioma cells, establishing the antioxidant system as a target of copper toxicity in tumoral cells. C6 and U-87 MG cells were exposed to CuSO (0-600 μM) for 24-48 h.

Copper dyshomeostasis and its relationship to AMPK activation, mitochondrial dynamics, and biogenesis of mitochondria: A systematic review of in vivo studies.

Introduction: Copper dyshomeostasis can be related to an increase in copper levels, resulting in toxicity, or to a decrease in tissues levels, impairing cuproenzyme activities. Inside cells, copper can be found in the cytoplasm and inside organelles, and the main organelle that compartmentalizes copper is the mitochondrion. This organelle can form networks and may fuse or fission from this, determining the mitochondrial fusion and fission processes, respectively.

Integration of ζ-deficient CARs into the CD3ζ gene conveys potent cytotoxicity in T and NK cells.

Chimeric antigen receptor (CAR)-redirected immune cells hold significant therapeutic potential for oncology, autoimmune diseases, transplant medicine, and infections. All approved CAR-T therapies rely on personalized manufacturing using undirected viral gene transfer, which results in nonphysiological regulation of CAR-signaling and limits their accessibility due to logistical challenges, high costs and biosafety requirements. Random gene transfer modalities pose a risk of malignant transformation by insertional mutagenesis.

Integration of ζ-deficient CARs into the gene conveys potent cytotoxicity in T and NK cells.

Unlabelled: Chimeric antigen receptor (CAR)-reprogrammed immune cells hold significant therapeutic potential for oncology, autoimmune diseases, transplant medicine, and infections. All approved CAR-T therapies rely on personalized manufacturing using undirected viral gene transfer, which results in non-physiological regulation of CAR-signaling and limits their accessibility due to logistical challenges, high costs and biosafety requirements. Here, we propose a novel approach utilizing CRISPR-Cas gene editing to redirect T cells and natural killer (NK) cells with CARs.