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Review Article

The Regulation Role of Ferroptosis Mechanism of Anti-Cancer Drugs and Noncoding RNAs

[ Vol. 30 , Issue. 14 ]


Mine Ensoy, Zehra Sena Bumin, Huda Abdirizak Jama and Demet Cansaran-Duman*   Pages 1638 - 1656 ( 19 )


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.


Ferroptosis, cell death, anti-cancer drugs, non-coding RNAs (ncRNAs), Sorafenib, miRNA.


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