Ferroptosis is an iron-dependent type of regulated cell death induced by hyperoxidation of polyunsaturated fatty acids within the phospholipids of the cytoplasmic membrane. According to recent studies, four key regulatory pathways of this process have been identified, with the glutathione pathway (SLC7A11/SLC3A2)/GSH/GPX4) being central and the most extensively studied. The functioning of all ferroptosis control systems is ensured by a multilayered network of protein-coding and regulatory genes, and disturbances in their expression may serve as a trigger for tumor cell transformation. Ferroptosis, along with other types of programmed cell death, plays a key role in the pathogenesis of many cancers, including non-small cell lung cancer (NSCLC). This review provides a detailed overview of the key molecular mechanisms of ferroptosis and summarizes the results of experimental studies demonstrating the involvement of ferroptosis-associated non-coding RNAs (microRNAs and long non-coding RNAs) in the development and progression of NSCLC. Special attention is given to the prospects of using anti-ferroptotic and pro-ferroptotic ncRNAs in NSCLC therapy, based on targeted modulation of their expression levels to induce ferroptosis in tumor cells.
Selezneva et al. (Wed,) studied this question.
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