AIFM2 (Apoptosis Inducing Factor Mitochondria Associated 2)

Beclin1 knockdown and DHODH overexpression can reduce DOX-induced liver injury by preventing ferroptosis and autophagy.

Recently developed technologies such as CRISPR-based functional genomics, metabolomics, and AI-powered modeling represent new-age tools in defining ferroptosis networks and precision therapeutics design. Integration of the regulation of normal physiological ferroptosis into cancer and diabetes therapy has the potential to redefine redox-targeted therapy and metabolic medicine. Antioxid. Redox Signal. 00, 000-000.

Clinically, higher CD36 expression correlated with the luminal androgen receptor (LAR) subtype of TNBC, known to exhibit a higher sensitivity to ferroptosis. Altogether, these data provide evidence for an essential role of the CD36 protein in the ferroptotic process induced by the saturated fatty acid PA, opening potential new therapeutic approaches promoting ferroptosis in the most aggressive breast cancers.

Cisplatin (DDP) is the first-in-class drug for advanced and non-targetable non-small-cell lung cancer (NSCLC). However, the effects were reversed by ferroptosis inhibitor ferrostatin-1 or deferoxamine in NSCLC cells. In summary, these results provide in vitro experimental evidence that PEM boosts the antitumor activity and increases the sensitivity of NSCLC cells to DDP by inducing ferroptosis.

Finally, the clinical relevance of ferroptosis in cancer therapy is discussed. Overall, this manuscript presents ferroptosis as a promising therapeutic avenue, offering new insights into its integration with existing cancer treatment strategies.

AIFM2 knockdown suppressed, whereas its overexpression enhanced, OSCC cell proliferation, migration, and invasion, while exerting minimal effects on cisplatin, palbociclib, or cold atmospheric plasma sensitivity. The LGBM-derived AIFM2 gene signature demonstrated strong prognostic predictive power. AIFM2 acts as an oncogenic driver in OSCC, regulated by tumor-suppressive miR-32-5p and miR-432-5p, and serves as a potential prognostic biomarker and therapeutic target.

As opposed to deletion of Gpx4 in all T cells, T cell deletion of Aifm2 did not impair antigen-specific CD8+ T cell responses. These results reveal an opportunity for targeting a regulator of ferroptosis that can not only directly target cancer cells but also simultaneously enhance anticancer immune responses without inciting autoimmunity.

To investigate the involvement of the NF-κB signaling pathway, HCT116 cells were treated with the NF-κB inhibitor Bay 11-7082...Mechanistically, TFPI-2 knockdown inhibited ferroptosis by promoting NF-κB pathway activity. This study reveals that TFPI-2 suppresses CRC progression by inducing ferroptosis through NF-κB signaling, providing new insights for future CRC therapy.

FSP1 acts as a metabolic safeguard maintaining ferroptosis resistance and drug tolerance in PTC. Its inhibition disrupts mitochondrial integrity and reinstates ferroptotic vulnerability, positioning FSP1 as a promising therapeutic target to eliminate drug-tolerant persister cells and reverse cisplatin resistance.

Two HCT116 lines were used to compare the effect related to cellular p53 protein status on the relative increase in tested gene expression. The modulation of p53 protein-dependent signaling pathways by the tested phenothiazine analogues was confirmed.

At present, traditional Chinese herbal medicine, combination therapy, and nano-delivery technology correlated with ferroptosis are being hotly studied by researchers in order to realize clinical translation of ferroptosis. In this review, we have summarized the core mechanisms of ferroptosis, ferroptosis differences from cuproptosis, its impact on cancers, and its translational implications in cancer therapy, helping readers quickly get the new information and horizons on them.