Abstract:Ferroptosis is a recently discovered type of cell death caused by the accumulation
of iron-dependent lipid peroxides and reactive oxygen species that differs significantly
from other cell death pathways such as apoptosis, necrosis, and autophagy. Ferroptosis
is essential in developing and treating ischemia-reperfusion injury, neurological diseases,
cancer, and other diseases. The ferroptosis mechanism, which can be induced by reagents
like erastin and glutamate, and suppressed by antioxidants such as vitamin E and deferoxamine
(DFO) chelators, can be regulated at the epigenetic, transcriptional, post-transcriptional,
and post-translational levels. A recent study has determined many non-coding
RNAs (lncRNA, miRNA, circRNA) that modulate ferroptotic cell death in cancer cells.
Furthermore, some anti-cancer drugs (Sorafenib, Sulfasalazine, Acetominofen, Lanperisone,
etc.) used in pre-clinical and clinical applications have been shown to induce ferroptosis
in various cancer types. However, in addition to the studies in the literature, it is necessary
to define novel molecules & non-coding RNAs and determine their effects on the
ferroptosis mechanism. Thus, it will be possible to develop effective and safe treatment
options.