The Regulation Role of Ferroptosis Mechanism of Anti-Cancer Drugs and Noncoding RNAs-Reference-Cited by-同舟云学术

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

Published:2023-04 Issue:14 Volume:30 Page:1638-1656
ISSN:0929-8673
Container-title:Current Medicinal Chemistry
language:en
Short-container-title:CMC

Author:

Cansaran-Duman Demet¹,Ensoy Mine¹,Bumin Zehra Sena¹,Jama Huda Abdirizak¹

Affiliation:

1. Biotechnology Institute, Ankara University, Kecioren, Ankara, Turkey

Abstract

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.

Publisher

Bentham Science Publishers Ltd.

Subject

Pharmacology,Molecular Medicine,Drug Discovery,Biochemistry,Organic Chemistry

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