FTH1 (Ferritin Heavy Chain 1)

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

However, overexpression of FTH1 suppressed ferroptosis and promoted tumor growth. Taken together, PRMT5/RBM15/ferritinophagy signaling can be a potential target for HCC.

FTH1 is a potential prognostic biomarker and therapeutic target for EC. Morin induces ferroptosis of EC cells by regulating FTH1-PI3K/AKT axis, providing a new candidate drug and theoretical basis for the treatment of EC.

Additionally, hMnL also shows good immunoprotective effects and long-term biosafety. These findings establish hMnL as a promising therapeutic platform that integrates targeted chemotherapy with immune modulation, offering a potent strategy to overcome immunosuppression and improve clinical outcomes in cancer.

Mechanistically, Lf-ChS-OX72 reduced FTH1 expression, indicating ferroptosis induction, with no influence on apoptosis. Lf-ChS microparticles provide a promising platform for OX72 delivery inducing ferroptosis-mediated cytotoxicity in doxorubicin-resistant sarcoma cells.

Data reveals a link between FTH1, labile iron, ROS, and IMiD resistance in MM cells.

On the other hand, it also activated iron-sulfur cluster assembly 2 (ISCA2)-mediated iron-sulfur cluster (ISC) assembly and iron starvation response to inhibit cuproptosis and ferroptosis. Collectively, our findings indicated the mechanism of the synergistic effect of ferroptosis and cuproptosis in the treatment of GC and presented a prospective therapeutic strategy through elucidating the molecular mechanism of ferroptosis and cuproptosis mediated by MTF1.

Finally, we found that silencing of NCOA4 prevented accumulation of TMR-Halo fragment and degradation of endogenous FTH1 under ferritinophagic conditions, confirming the specificity of our assay. Together, the HaloTag-FTH1 tool we generated can be used to specifically detect and quantitate ferritinophagy in mammalian cells with a fluorescent Halo-ligand, and this approach can be instrumental in studies focusing on cellular iron metabolism.

EA can improve the learning and memory abilities of MCAO/R rats, and its mechanism may be related to the inhibition of ferritinophagy mediated by the cGAS-STING signaling pathway.

Our findings reveal a novel role for VCPKMT as a regulator of ferroptosis sensitivity in CRC, highlighting the VCPKMT-VCP-HDAC1 axis as a potential therapeutic target for CRC treatment.

Our results demonstrate that NSUN2 facilitates leukemogenesis by increasing FTH1 expression and enhancing global protein synthesis in an m5C-dependent manner. Targeting NSUN2 might provide a promising therapeutic strategy for B-ALL.

BBR triggers ferroptosis-mediated energy metabolism disorder by inhibiting Gli1/STAT3-FNR axis. This work provides a mechanistic support for BBR anti-CRC indications, and suggests an encouraging approach for treating CRC.