SLC7A11 (Solute Carrier Family 7 Member 11)

Furthermore, we identify sodium 2, 2-dichloroacetate (DCA) as a novel inhibitor of USP30, and DCA inhibits CRC serine synthesis and tumor growth. Clinically, USP30, FTO, PHGDH, and PSAT1 levels are highly correlated in CRC tissues. This study provides mechanistic insights into how USP30 senses serine/glycine levels to regulate serine synthesis via the FTO-PHGDH/PSAT1 axis, offering a potential therapeutic strategy for targeting serine/glycine metabolism in cancer.

By integrating mechanistic insights with therapeutic applications, this study not only elucidates the dynamic complexity of ubiquitin-mediated regulatory networks but also proposes innovative strategies leveraging Ub/Ubl modifications for targeted cancer therapy. These findings provide a foundational theoretical framework and actionable research directions for advancing precision medicine in oncology.

BTW alleviates UC-related inflammation and intestinal barrier damage by modulating apoptosis, mitophagy, and ferroptosis, while mitigating oxidative stress.

Furthermore, curcumin significantly inhibited tumor growth (p=0.039) and exhibited a synergistic antitumor effect with oxaliplatin in vivo. This study comprehensively elucidates the molecular mechanisms by which curcumin exerts its therapeutic effects in CRC via modulation of ferroptosis and Wnt/β-catenin signaling pathway. These findings provide novel mechanistic insights and support the translational potential of curcumin in preclinical and clinical frameworks.

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.

In an orthotopic TNBC mouse model, xanthatin significantly suppressed tumor growth without causing systemic toxicity. Collectively, our findings provide the first demonstration that xanthatin directly targets CISD1 at the Trp-75 site to trigger ferroptosis and mitophagy, highlighting its promise as a therapeutic candidate for TNBC.

Repurposed drugs such as flubendazole and the ezetimibe derivative L14-8, along with natural compounds including evodiamine and luteolin, demonstrate translational potential for ferroptosis induction. Collectively, ferroptosis represents a promising therapeutic vulnerability for precision treatment of advanced prostate cancer.

Ion channels and ecDNA are central to the disease progression and treatment resistance of PCa through regulation of EMT, CSC phenotype, and tumor microenvironment (TME) interactions. Targeting the drivers-through ion channel modulators, ferroptosis induction, and ecDNA-targeting interventions (BET/HDAC inhibitors, CRISPR-based methods) offers a promising way to overcome resistance. Integration of multi-omics, and combination treatments will be key to construct precision medicine strategies and improve clinical outcomes in advanced PCa.

These findings reveal a pathway underlying EG-induced transient liver damage and suggest a possible mechanism of recovery, thereby providing new insights into EG poisoning.

This study found that HSF4 overexpression markedly attenuated Erastin-induced cell death and mitochondrial damage in HT29 and HCT116 cells...In vivo experiments, MBOAT1/2 knockdown effectively reduced tumor volume and downregulated the number of Ki-67-positive cells, GPX4, and SLC7A11, while upregulating ACSL4. In conclusion, HSF4 alleviates ferroptosis in CRC cells and facilitates tumor progression by upregulating MBOAT1/2 transcription, thereby limiting lipid peroxidation and Fe2+ accumulation.

These findings support a model in which CBD downregulates HER2 and, in a HER2-dependent context, promotes paraptosis and ferroptosis. In addition, docking and molecular dynamics analyses suggested a potential interaction between CBD and HER2, providing mechanistic insights into possible molecular recognition relevant to HER2-positive breast cancer.

This review summarizes recent discoveries on the NK-ferroptosis axis, delineates the molecular and cellular mechanisms governing their crosstalk in the TME, and explores therapeutic opportunities to leverage this pathway for cancer treatment. Understanding this regulatory network could inform the development of innovative immunometabolic interventions to improve current immunotherapy outcomes.