Review examines the role of ferroptosis, an iron-dependent form of cell death, in prostate cancer, exploring its underlying molecular mechanisms and potential for targeted therapeutic strategies.
By Dr. Chinta SidharthanApr 17 2024Reviewed by Susha Cheriyedath, M.Sc. In a recent review published in the journal Nature Reviews Urology , researchers examined the molecular mechanisms and metabolic processes that drive ferroptosis — a form of cell death that plays a significant role in prostate cancer . They also connected pathways involved in ferroptosis to the metabolic reprogramming that occurs in prostate cancer cells to highlight potential avenues of targeted therapeutic interventions.
Recent research has found that a pathway of regulated cell death, called ferroptosis, plays a significant role in the development of prostate cancer. Ferroptosis differs from the other forms of cell death, such as autophagy, apoptosis, and necrosis, in that it is iron-dependent and is driven by lipid peroxide build-up. Studies have found that the suppression of ferroptosis is linked to tumor pathogenesis, especially in prostate cancer.
Cells contain various intrinsic systems to circumvent lipid peroxidation and ferroptosis. The classical method involves the use of glutathione and glutathione peroxidase 4 to decrease the levels of lipid hydroperoxides, preserving the integrity of the phospholipid bilayer and preventing ferroptosis. Inhibition of ferroptosis can also occur through ferroptosis suppressor protein 1 or dihydroorotate dehydrogenase.
The review discussed various mechanisms through which the susceptibility of cancer cells to ferroptosis could be exploited as potential treatment avenues for advanced cancers. Targeting the defense mechanisms that inhibit ferroptosis is a promising approach. Studies have suggested that targeting the glutathione peroxidase 4 inhibition mechanism could induce ferroptosis in cancer cells that do not respond to other treatment options.
Ferroptosis Prostate Prostate Cancer Research Androgen Apoptosis Autophagy Cell Cell Death Chemotherapy Fatty Acids Imaging Immunotherapy Membrane Metabolism Metastasis Necrosis Oxygen Protein Radiotherapy Receptor Urology
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