Abstract
A novel kind of nonapoptotic, iron-dependent cell death brought on by lipid peroxidation is known as ferroptosis. Numerous pathological processes, including neurotoxicity, neurological disorders, ischemia-reperfusion damage, and particularly cancer, have been demonstrated to be influenced by changes in the ferroptosis-regulating network. Recent studies have established the critical roles that ferroptosis can play in cancer development and the evolution of resistance to standard chemoradiotherapy, thus suggesting that ferroptosis may be a feasible therapeutic strategy for cancer management. Gene expression may be regulated at the transcriptional and posttranscriptional levels by long noncoding RNAs (lncRNAs). They have been implicated in tumorigenesis. Some lncRNAs participate in the biological process of ferroptosis, which represents an exciting alternative to regulate ferroptosis as a means of cancer therapy. Even though there is evidence that lncRNAs have a mechanistic role in the ferroptosis of cancer cells, research on the mechanism and potential treatments for these lncRNAs is still lacking. We elucidate the potential mechanisms by which lncRNAs modulate ferroptosis in cancer and examine the promise and challenges of employing lncRNAs as novel therapeutic targets in cancer.
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