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Balihodzic, A; Prinz, F; Dengler, MA; Calin, GA; Jost, PJ; Pichler, M.
Non-coding RNAs and ferroptosis: potential implications for cancer therapy.
Cell Death Differ. 2022; 29(6):1094-1106 Doi: 10.1038/s41418-022-00998-x [OPEN ACCESS]
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Leading authors Med Uni Graz
Balihodzic Amar
Pichler Martin
Co-authors Med Uni Graz
Dengler Michael
Jost Philipp
Prinz Felix

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Ferroptosis is a recently defined form of regulated cell death, which is biochemically and morphologically distinct from traditional forms of programmed cell death such as apoptosis or necrosis. It is driven by iron, reactive oxygen species, and phospholipids that are oxidatively damaged, ultimately resulting in mitochondrial damage and breakdown of membrane integrity. Numerous cellular signaling pathways and molecules are involved in the regulation of ferroptosis, including enzymes that control the cellular redox status. Alterations in the ferroptosis-regulating network can contribute to the development of various diseases, including cancer. Evidence suggests that ferroptosis is commonly suppressed in cancer cells, allowing them to survive and progress. However, cancer cells which are resistant to common chemotherapeutic drugs seem to be highly susceptible to ferroptosis inducers, highlighting the great potential of pharmacologic modulation of ferroptosis for cancer treatment. Non-coding RNAs (ncRNAs) are considered master regulators of various cellular processes, particularly in cancer where they have been implicated in all hallmarks of cancer. Recent work also demonstrated their involvement in the molecular control of ferroptosis. Hence, ncRNA-based therapeutics represent an exciting alternative to modulate ferroptosis for cancer therapy. This review summarizes the ncRNAs implicated in the regulation of ferroptosis in cancer and highlights their underlying molecular mechanisms in the light of potential therapeutic applications.
Find related publications in this database (using NLM MeSH Indexing)
Apoptosis - genetics
Cell Death - physiology
Ferroptosis - genetics
Humans - administration & dosage
Neoplasms - drug therapy, genetics
Oxidation-Reduction - administration & dosage
Reactive Oxygen Species - metabolism

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