STEAP3 (STEAP3 Metalloreductase)

Overall, these findings suggest that GL-V9 induces apoptosis in SCLC by targeting STEAP3 for proteasomal degradation, thereby disrupting the STEAP3-CISD2 axis and promoting oxidative stress-driven cell death. This study identifies a previously unrecognized redox regulatory pathway in SCLC and proposes a potential therapeutic strategy centered on selective induction of oxidative stress.

Moreover, Kyoto encyclopedia of genes and genomes pathways, such as Calcium signaling, MAPK signaling, cAMP signaling, and Rap1 signaling, were significantly enriched. In conclusion, our model, based on AS genes, effectively predicts glioma prognosis, identifying NRG1 as a significant marker.

We expanded the phenotype to include cytopenia and neonatal HLH. Our report on two affected male siblings highlights the expanded phenotype, clarifies the phenotypic spectrum of STEAP3, and broadens its genetic inheritance, ultimately providing a clinical and molecular workup for neonatal patients with unexplained HLH.

Upregulation of STEAP3 suppresses ferroptosis by increasing glutathione levels and reducing lipid peroxidation, ultimately promoting tumor proliferation and gemcitabine resistance. Our study identifies the USP10-IGF2BP3-STEAP3 axis as a critical mechanism underlying chemoresistance in pancreatic cancer, suggesting that targeting USP10 may offer a promising therapeutic strategy for overcoming gemcitabine resistance.

By promoting iron-dependent cell death and suppressing migratory capacity, Berberine may overcome resistance to conventional therapies and reduce metastatic progression. Its natural origin and prior safety profile support drug repurposing opportunities, though challenges such as poor bioavailability and systemic toxicity must be addressed. These findings provide a foundation for biomarker-driven preclinical and early clinical evaluations. How to cite this article: Alassiri S. Berberine Induces Ferroptosis and Impairs Migration via Glutathione Peroxidase4/Six-transmembrane Epithelial Antigen of Prostate3 Signaling Pathway in Oral Cancer Cells. J Contemp Dent Pract 2025;26(11):1050-1059.

Critically, targeted knockdown of STEAP3 remarkably inhibited TNBC cells proliferation, migration and xenograft tumor growth. These findings unveil a critical pro-tumorigenic copper-driven pathway-distinct from cuproptosis-operating through STEAP3/copper/CDK16/JAK1 axis, and highlight STEAP3 as a promising therapeutic target for TNBC.

Fer-1 alleviated these effects. These findings establish ferroptosis as a novel mechanism underlying DEHP/MEHP-induced β cell dysfunction and provide new insights into the role of PAEs, environmental pollutants, in diabetes pathogenesis.

This study reveals how cancer cells abnormally upregulate SLC7A11 by hijacking multi-level mechanisms, gaining strong antioxidant/anti ferroptotic abilities, which are the core basis for their survival, proliferation, and resistance to treatment. This study also identified SLC7A11 as a convergence point for multiple key pathways, making it an ideal hub target for intervening in cancer and overcoming drug resistance.

Furthermore, (+)-strebloside suppressed NHL proliferation through the mitogen-activated protein kinase (MAPK) pathway, and extracellular signal-regulated kinase (ERK) inhibition diminished the proliferation-inhibitory activity induced by (+)-strebloside. These findings indicate that (+)-strebloside presents promising therapeutic potential for NHL treatment.

In nude mouse xenograft models, IGF2BP2 knockdown inhibited tumor growth and altered the expression of CP, GPX4, and ferroptosis markers. Collectively, our findings suggest that IGF2BP2 may serve as a therapeutic target in NPC by modulating m6A modification and CP stability to inhibit ferroptosis.

In summary, these findings revealed that the lncRNA STEAP3-AS1 interacts with its parental gene STEAP3 to regulate H3K18la through BRG1, resulting in changes in chromatin accessibility, thereby driving ERG enrichment an the MMP9 promoter to activate MMP9 transcription and promote CRC liver metastasis. Our findings reveal a novel mechanism by which the lncRNA STEAP3-AS1 promotes CRC metastasis from an epigenetic perspective.

As a key mediator connecting SETDB2 and iron metabolism in ESCC progression, TFRC knocking-down can rescue cell proliferation rate changes caused by SETDB2 knocking-down as well. Our results not only elucidated the role of SETDB2 methyltransferase in ESCC tumorigenesis by regulating cellular iron homeostasis through H3K9me3 modification, but also highlighted the potential of iron chelation-based anticancer therapy for ESCC patients with SETDB2 copy number deletion in clinical treatment.