SLC3A2 (Solute Carrier Family 3 Member 2)

According to in vivo experiments, UA inhibited CRC tumor growth by regulation of above genes. This study demonstrated that UA could effectively inhibit CRC proliferation by inducing ferroptosis via regulation of system xc- subunits and miR-214-3p/Stat3/GPX4 axis, suggesting UA could serve as a promising anti-colorectal cancer candidate requiring further validation and optimization.

The combination of ANPEP silencing and sorafenib treatment showed a synergistic effect in inhibiting liver cancer progression. Finally, clinical data and mouse models demonstrated that chronic stress drove liver tumor progression via ANPEP-regulated SLC3A2. These findings reveal unanticipated communication between chronic stress and metabolic reprogramming during liver cancer progression, providing potential therapeutic implications for liver cancer.

This new purification method results in LDN with high purity (more than 90%) and viability (more than 96%) in a short time period. This method can easily be scaled up to obtain large numbers of pure LDN to evaluate LDN functions in different diseases through biochemical or other omics analysis.

In line with this, HnRNPU deletion induced ferroptosis and increased sensitivity to RSL3 treatment and cysteine deprivation...Findings demonstrate that HnRNPU promotes proliferation and inhibits ferroptosis by regulating the mRNA stability of SLC7A11 and SLC3A2. Targeting HnRNPU is a potential therapeutic approach for COAD treatment.

These findings indicate that, beyond the canonical GPX4 pathway, the xCT/CD98 complex can inhibit ferroptosis via the TRIM21/RACK1/FPN1 axis. Targeting RACK1 offers a potential therapeutic strategy to sensitize tumors to ferroptosis and overcome therapy resistance across multiple cancer types and in people with cancer.

Given that lipid metabolism regulates ferroptosis by controlling cellular processes associated with phospholipid peroxidation. The TRIM15/YY2/FOXRED1 axis demonstrates that it modulates SLC3A2 expression via the mTOR/c-MYC pathway, thereby regulating GPX4 levels to influence EAC sensitivity to ferroptosis-inducing compounds and proposing a therapeutic strategy for EAC.

This review provides a comprehensive overview of the molecular mechanisms of ferroptosis and summarizes experimental evidence demonstrating involvement of the ferroptosis-associated non-coding RNAs (microRNAs and long non-coding RNAs) in the development and progression of NSCLC. Special emphasis is placed on the potential application of anti-ferroptotic and pro-ferroptotic non-coding RNAs in NSCLC therapy, focusing on targeted modulation of their expression to induce ferroptosis in tumor cells.

CLDND1 marks an immune-cold, ferroptosis-resistant phenotype in OSCC and independently portends adverse outcomes. Targeting CLDND1-linked circuitry-alone or combined with ferroptosis induction-merits further translational evaluation for OSCC diagnosis and therapy.

HOXA13 drives PCa progression by transcriptionally activating SLC7A11 and SLC3A2, which suppress ferroptosis and enhance proliferation and metastasis. The findings highlighted sh-HOXA13 promoting ferroptosis as a potential strategy for PCa treatment.

In this study, we constructed an MFRS model to predict patient prognosis and therapeutic response. This study also preliminarily reveals the roles of M2Ms and ferroptosis in HNSCC patients and provides potentially novel insight for treatment.

To address these limitations, we developed a magneto-photo-acoustic responsive nanoplatform (MnFe2O4-erastin-perfluoropentane nanoparticles [MEPNPs])...This work establishes a novel "theranostic-immunomodulatory" paradigm that integrates magnetic targeting, ferroptosis potentiation, and immunogenic-cell-death-mediated immune memory. By orchestrating physical energy conversion, MEPNPs provide a spatially focused and immunologically amplified strategy to overcome TNBC therapeutic resistance.

Notably, the immune-sensitive phenotypes seen in METTL5-KO tumors can be reversed by either ATF4 overexpression or ferroptosis inhibition. These findings underscore the central role of the METTL5/ATF4/ferroptosis axis in controlling OC responses to immunotherapy.