Here is reading for this snowy day: Congrats to Hanna Feinsod on publication of our perspective in Ferroptosis & Oxidative Stress on 3 major unanswered questions in #ferroptosis! https://www.sciexplor.com/articles/fos.2026.0015
Fundamental mechanism of ferroptosis: Three unanswered questions

Ferroptosis, an iron-dependent form of regulated cell death (RCD) driven by lipid peroxidation, has been extensively studied since its conceptualization in 2012 and has been suggested as a therapeutic target in many cancers and degenerative diseases. However, three fundamental questions remain unanswered about ferroptosis. First, the mechanisms by which cells execute death during ferroptosis remain elusive: The key role of lipid peroxides in triggering ferroptosis is established, but how this results in the death of a cell remains unclear. Second, the physiological role of ferroptosis throughout the human life cycle is unclear; currently, there is evidence for ferroptosis in early development, immunity, aging, and tumor suppression, but not in many other aspects of physiology. Third, and finally, the intersection between ferroptosis and other RCD modalities, such as apoptosis, necroptosis, pyroptosis, and autophagic cell death, is necessary for understanding how ferroptosis integrates into networks controlling cellular fate. Addressing these gaps in knowledge is essential for building a comprehensive understanding of this mode of cell death, as well as translating ferroptosis knowledge into effective therapeutics.

Researchers show how a defect in the #enzyme #GPX4 can trigger #ferroptosis and lead to neuronal loss in certain forms of #dementia. The work provides new insights into cell protection mechanisms: http://go.tum.de/142494

📷T.Orschmann & S. Lorenz

Defective enzyme causes nerve cells to die

Researchers have discovered a protective mechanism in nerve cells that offers new targets for future therapies—especially for dementia.

Congrats to Jenny and Liam on our Prevew in Molecular Cell on the excellent paper by Yaqin Deng, Jin Ye et al in the same issue describing a new protection mechanism against #ferroptosis by #DHA — Here is a free download: https://authors.elsevier.com/a/1loAH3vVUPVb4P @MolecularCell @Columbia
Exploiter la chimie du fer pour battre le cancer

Les travaux menés à l’Institut Curie par l’équipe de Raphaël Rodriguez « Chimie et biologie du Cancer » ont révélé un nouveau point d’entrée pour induire la mort des cellules à potentiel métastatique en lien avec le métabolisme du fer. Avec Marcus Conrad, pionnier de la ferroptose, et Stuart Schreiber, fondateur de la chemical biology moderne, ils conceptualisent ensemble de nouvelles approches thérapeutiques dans un article publié dans Molecular Cell.

Institut Curie

New Publication Alert!
"The Effective Stress Response Role of p53 in Inducing Ferroptotic Cell Death"


Link:
https://lnkd.in/gPA6qVdC


#p53 #ferroptosis #stress #celldeath

Breakthrough molecules exploit cancer cells' iron metabolism to induce self-destruction, offering hope against metastasis. #CancerResearch #Ferroptosis #MedicalInnovation

https://geekoo.news/iron-molecules-strike-back-at-resistant-cancer-cells/

Iron Molecules Strike Back at Resistant Cancer Cells | Geekoo

French researchers have unveiled a new class of molecules that trigger ferroptosis in drug-resistant cancer cells, offering a promising strategy to combat metastasis and improve patient outcomes.

Geekoo
A Pan-Cancer Analysis of Ferroptosis-Related Gene Arachidonic Acid 15-Lipoxygenase-1 (ALOX15): Its Prognostic and Immunotherapeutic Values - #ferroptosis #bioinformatics #prognosis #pancancer #ALOX15 #biologicalfunctions #immune - https://link.springer.com/article/10.3103/S0095452724050141
A Pan-Cancer Analysis of Ferroptosis-Related Gene Arachidonic Acid 15-Lipoxygenase-1 (ALOX15): Its Prognostic and Immunotherapeutic Values - Cytology and Genetics

Abstract Background. Emerging research has identified ferroptosis as a novel form of programmed cell death, and Arachidonic acid 15-lipoxygenase-1 (ALOX15) stands out as a pivotal gene in mediating this process. Nonetheless, the role of ALOX15 in human tumors remains elusive. Methods. We utilized TIMER 2.0 to investigate the differential expression profiles of ALOX15 between pan-cancer and normal tissues. Further data from the TCGA, GEPIA, UALCAN, HPA, and CPTAC databases were analyzed to verify the levels of mRNA, protein expression, and promoter methylation across various cancer types. The survival prognosis, clinical features, and genetic alterations of ALOX15 were also evaluated. GO/KEGG enrichment analyses and single-cell transcriptome sequencing were employed for functional enrichment analysis. The gene mutation of ALOX15 and its prognostic value were analyzed using the cBioPortal platform. Finally, the relationship between ALOX15 and immune cell infiltration, Immune Checkpoints (ICKs), genomic instability, and drug sensitivity was further explored using GSCA. Results. Our findings revealed that the transcription and protein expression of ALOX15 were significantly reduced in HNSC, LUAD, LUSC, SKCM, KICH, and THCA, while they were up-regulated in ESCA, LIHC, PRAD, and UCEC. Notably, the expression of ALOX15 had prognostic value for certain cancers, including LUAD, LUSC, LIHC, KIRC, HNSC, THCA, and LGG. Additionally, ALOX15 expression was markedly correlated with clinical characteristics, immune cell infiltration, ICKs, genomic instability, and antitumor drug sensitivity in various tumors. Gene mutations of ALOX15 and their prognostic value were discovered in pan-cancers. Furthermore, GO/KEGG analysis and single-cell transcriptome sequencing indicated that ALOX15 was significantly associated with cancer-related pathways. Conclusion. Our comprehensive pan-cancer analysis shed light on the role and significance of ALOX15, suggesting its potential as a prognostic and immunotherapeutic marker for pan-cancer. These findings may provide new directions and evidence for cancer therapeutics.

SpringerLink