SLC7A11 (Solute Carrier Family 7 Member 11)

These microRNAs have demonstrated to have both pro-ferroptotic and anti-ferroptotic effects across a variety of disease models through in-silico predictions and experimental validation in each case, depending on the dynamics of their expression. Therapeutic interventions using microRNA-mimics, antagomirs, and adjunct therapeutic methods utilising natural compounds show the potential to control ferroptosis by regulating GPX4, thus providing new opportunities for the treatment of ferroptosis-related diseases.

In conclusion, a metabolic cycle occurs in MM BM microenvironment, where Gln-auxotroph MM cells extrude glutamate that is converted into Gln by MSC, sustaining in turn MM anabolism through Gln secretion. The inhibition of this metabolic trade-off impairs MM cell growth, thus highlighting novel potential, niche-oriented therapeutic targets.

Curcumin can inhibit the viability and induce ferroptosis in CRC cells, while leucovorin is known to enhance the cytotoxic effects of fluorouracil in the same cells. However, additional leucovorin pre-treatment did not display further benefits compared with curcumin and leucovorin co-treatment. The findings of the present study suggested that curcumin and leucovorin may serve as a potential regimen for the treatment of CRC.

High expression of UXS1 serves as a prognostic biomarker for HCC. UXS1 knockdown suppresses HCC malignant progression, at least partially, by inducing ferroptosis via the SLC7A11/GPX4 axis. These findings suggest UXS1 is a potential therapeutic target and a novel ferroptosis checkpoint in HCC.

Moreover, activated T cells secrete IFN-γ, which suppresses SLC7A11 expression and reduces intracellular glutathione synthesis, therefore establishing a self-amplifying ferroptosis loop. As envisaged, this "shock and awaken" strategy, integrating PCT with a partially degradable design, effectively reprograms the immunosuppressive TME, improves antitumor efficacy, and inhibits lung metastasis, highlighting its promise for piezocatalytic immunomodulation.

Significant synergistic effects were observed when GCLC inhibitors were combined with agents targeting the GSH synthesis pathway, specifically SLC7A11 inhibitors and the glutaminase inhibitor telaglenastat...These findings highlight the vulnerability of glutathione metabolism in SMARCB1-deficient cancers, suggesting that a GCLC inhibitor may be a promising therapeutic option. This study provides a preclinical foundation for the development of effective treatment strategies for SMARCB1-deficient cancers, including combination therapies, and supports further investigation toward future translational applications.

FAT4 may enhance ferroptosis sensitivity in HCC by suppressing GPX4 and SLC7A11 expression, potentially by inhibiting PI3K/AKT signaling. Thus, this study presents FAT4 as a biomarker associated with tumor progression and a potential determinant for overcoming ferroptosis resistance in HCC.

This study identified a ferroptosis transcriptional program that is deregulated in two independent transcriptome cohorts. At the single-cell level, these alterations, linked to oxidative stress response, revealed insights into neuronal differentiation within human hepatoblastoma tumors.

This study demonstrated that the DNA tetrahedron-based nanocarrier functionalized with AS1411 aptamer effectively delivers vorinostat and enhances its dual action on ferroptosis and EMT in GC. This targeted nanoplatform represents a promising strategy for precise and combinatory GC therapy.

Selenoenzyme glutathione peroxidase 4 (GPX4) controls this process by reducing lipid peroxides and can be pharmacologically inhibited by agents such as RSL3 and JKE1674...However, by assessing expression of iron regulatory genes as well as employing two orthogonal approaches to measure labile iron, we found that the LIP did not measurably increase during ferroptosis induction with GPX4 or SLC7A11 inhibition. These findings suggest that the LIP does not expand upon pharmacologically initiated ferroptosis, despite the potentiating effect of exogenous iron supplementation.

COS-SA-SeNPs exert antitumor effects by disrupting redox homeostasis and inducing ferroptosis through the simultaneous impairment of cellular antioxidant defenses. This study not only provides an alternative candidate for nutritional selenium supplementation but also offers fresh perspectives on ferroptosis-mediated cancer therapy through the enhancement of redox imbalance.

SIGNIFICANCE STATEMENT: The discovery of disulfidptosis enriches understanding of programmed cell death, providing a foundation for targeting SLC7A11-mediated cystine metabolism and other key pathways to treat various diseases and offering new approaches for managing pathological processes previously considered intractable. As molecular mechanistic understanding advances, these emerging therapeutic strategies may open new research avenues, although clinical translation and efficacy require further validation.