![]() SLC7A11/xCT is a transporter subunit of system Xc − that imports cystine in exchange for glutamate in an ATP-independent manner. The most established cause of lipid peroxidation is the regulation of cellular levels of glutathione (GSH) via the SLC7A11/xCT and the antioxidant enzyme glutathione peroxidase 4 (GPX4) axis. Ferroptosis is linked to the accumulation of lipid peroxides and iron, which can be caused by the failure of antioxidant activity through lipid peroxidation. ![]() These results may be useful in predicting the ferroptosis response in NSCLC as well as drug resistant cancer cells.įerroptosis is a novel type of iron-dependent, oxidative damage-related cell death that is distinguished from other types of programmed cell death based on its genetic, morphological, and biochemical characteristics 1. Taken together, RS元-induced ferroptosis depends on the regulation of GPX4-Nrf2/HO1 in NSCLC cells. GPX4 knockdown had a similar effect on ferroptosis phenotypes as RS元. Furthermore, RS元 induced autophagosomes but disrupted the formation of autolysosomes with lysosomal membrane destabilization. RS元 induced ferroptosis by promoting lipid peroxidation, elevating intracellular LIP concentration and ROS level, and blocking GSH-to-GSSH conversion through the inhibition of GPX4 and induction of Nrf2/HO1. The sensitivity of NSCLC cells to RS元 induced death was dependent on GPX4 expression levels the effect of RS元 was reversed by ferrostatin-1 (a ferroptosis inhibitor) but not by Z-VAD-FMK, chloroquine, bafilomycin A1, or necrostatin-1. RS元 induced cell death more effectively in NSCLC cells than erastin, with limited cytotoxicity in BEAS-2B normal bronchial epithelial cells. Here, we investigated the anticancer effects of ferroptosis inducers erastin and RS元 on non-small cell lung cancer (NSCLC) cells. Recently, it has been suggested that ferroptosis can be an effective way to induce cancer cell death, although the specific relevance and mechanism of ferroptosis have not been fully elucidated. Ferroptosis can be induced by inhibiting antioxidant enzymes GPX4 or system Xc −, increased intracellular iron concentrations, and lipid peroxidation.
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