FTL (Ferritin Light Chain)

Conclusively, the findings indicate that histone methylation-driven TRMT6 is crucial for the translation of FTH1 and FTL, which bridges the understanding of m1A tRNA modification and ferroptosis. These results highlight TRMT6 as a novel potential therapeutic target for TNBC.

Mechanism studies have shown that FTL promotes ESCC development and metastasis via NRF2 pathway and inhibits ferroptosis via NCOA4 protein. In vivo treatment, Brusatol, was found to inhibit FTL expression and have a significant inhibitory effect on ESCC growth and metastasis.

In rare circumstances, however, ferritin levels may be primarily elevated due to a genetic cause. We report a case of a three-year-old male patient with incidentally detected hyperferritinemia who was found to harbor the c.-168G>T mutation in the FTL gene, confirming hereditary hyperferritinemia-cataract syndrome (HHCS). This case is distinguished by a unique four-generation family history of early-onset cataracts and elevated ferritin levels, underscoring the hereditary and novel nature of this disorder.

Moreover, the specific NRF2 inhibitor ML385 was able to reverse the alterations in GSH, Fe2+, and MDA levels induced by LBP. In conclusion, our research results indicate that LBP induces ferroptosis by activating the NRF2/HO-1 signaling pathway.

Co-treatment with Tat-beclin 1 and erastin enhanced BECN1-SLC7A11 complex formation, more strongly inhibited system Xc⁻, enhanced lipid peroxidation, inhibited the Nrf2-Keap1 signaling pathway and significantly suppressed tumor growth in vivo. Tat-beclin 1 promotes ferroptosis and tumor suppression in NSCLC by activating BECN1 and inhibiting SLC7A11-mediated system Xc⁻ activity.

In vivo studies have shown that DARP_9-29-FTLsh-EC1/MMAE is selectively accumulated in HER2/EpCAM-positive tumors in a mouse xenograft model causing significant tumor reduction. Our results demonstrate that bispecific targeting opens new prospects for the development of precise anticancer therapy.

In addition, Hv1 knockdown mitigated interleukin-1β secretion and suppressed ferroptosis markers (ferritin heavy chain/ferritin light chain, CCAAT/enhancer binding protein homologous protein, glucose-regulated protein 78, etc.) in vitro, suggesting the involvement of an Hv1-reactive oxygen species-glucose-regulated protein 78 axis in diabetic demyelination. We highlight the translational implications of these findings and recommend future studies employing microglia-specific Hv1 deletion models, longitudinal cognitive assessments and preclinical evaluation of pharmacological Hv1 inhibitors.

Overall, our findings highlight the significant impact of EBV on ferritin, underscoring a previously unrecognized role of ferritin in the progression of EBVaGC. This novel pathway could offer new therapeutic targets for the treatment of EBVaGC.

Our study identifies the NRF2-GSTT2-GPX4 ferroptosis regulatory axis, demonstrating that GSTT2 is a negative regulator of ATO-induced ferroptosis. Targeting this axis may represent a promising therapeutic strategy for overcoming chemotherapy in PDAC.

Finally, ferritin should be regarded as a regulator of the dysfunctional iron metabolism that causes increased iron levels in AML cells, and it is important for cell survival through its function during the initial steps of ferroptosis. Thus, ferritin is not only an adverse prognostic biomarker, but also an important regulator of AML cell proliferation, survival and chemosensitivity and the targeting of iron metabolism/ferroptosis is, therefore, a possible strategy in AML therapy.

Iron chelators such as Deferoxamine (DFO), Deferasirox (DFX), and Dp44mT have demonstrated significant promise in cancer treatment by inducing iron deficiency within tumor cells. This review explores recent advancements in nanotechnology aimed at targeting iron metabolism in cancer cells and discusses their potential applications in cancer treatment strategies.

SCARA5 up-regulation enhanced ferroptosis in CC by inhibiting mitochondrial damage. We conclude that SCARA5 promoted ferroptosis in CC cells by inhibiting FTL ubiquitination-induced mitochondrial damage, which may contribute to the treatment of CC.