DMRT1 (Doublesex And Mab-3 Related Transcription Factor 1)

In contrast, under standard low-Cu conditions, CTR1 remains required for cellular Cu uptake and CuCOX metallation. Together, these findings define context-dependent Cu trafficking pathways in renal cancer and establish SEC-ICP-MS as a sensitive platform for assessing CuCOX metallation and mitochondrial metabolism, with potential applications in biomarker discovery and therapeutic targeting in RCC.

Cisplatin (DDP) is the first-in-class drug for advanced and non-targetable non-small-cell lung cancer (NSCLC). However, the effects were reversed by ferroptosis inhibitor ferrostatin-1 or deferoxamine in NSCLC cells. In summary, these results provide in vitro experimental evidence that PEM boosts the antitumor activity and increases the sensitivity of NSCLC cells to DDP by inducing ferroptosis.

Alterations associated with the formation of a somatic-type malignancy and/or the development of cisplatin resistance include TP53 mutations or MDM2 gene amplifications as well as epigenetic alterations...Additionally, we will provide guidance on how to examine a testicular tumour specimen histopathologically to reach an accurate diagnosis. Finally, we will outline the importance of the content of a histopathological report for the urologists and oncologists.

Overall, this study indicates that regulating iron homeostasis to inhibit ferroptosis is related to the therapeutic effect of 6-gingerol against CINV.

ID is closely associated with aggressive tumor biology, suboptimal response to neoadjuvant therapy, and impaired postoperative recovery. Dysregulation of iron homeostasis and ferroptosis pathways in ID patients may contribute to CRC progression. These findings highlight ID as a potential biomarker for risk stratification and suggest that targeting iron metabolism could improve therapeutic outcomes in CRC management.

Treatment with verapamil, an L-type Ca2+ channel inhibitor, significantly reduced Cd uptake in UMR-106 cells...However, the degree of reduction ranged from 15 to 35%, indicating that no single pathway makes a predominant contribution. These findings suggest that diverse pathways, encompassing metal transporters and Ca2+ channels, contribute to Cd uptake in UMR-106 cells, although no single pathway predominates.

Pre-treatment with BA markedly suppressed LPS and FeSO4-induced upregulation of pro-inflammatory cytokines, ferroptosis, apoptosis, and dopaminergic cell death markers. These findings suggest that BA exerts neuroprotection by modulating the GPX4/Nrf2/Keap-1/HO-1 antioxidant defense and p38MAPK/NF-κB inflammatory signaling pathways, highlighting its potential as a therapeutic agent for oxidative stress-related neurodegenerative conditions, such as Parkinson's disease (PD).

In vivo experiments further validated that KRT15 overexpression promoted tumor growth, EMT, Wnt/β-catenin signaling pathway, and irradiation resistance, but repressed the ferroptosis. Collectively, KRT15 may facilitate tumor growth, invasion, EMT, and radioresistance but represses ferroptosis in a Wnt/β-catenin signaling-related way, suggesting its potency as a treatment target for breast cancer management.

This study offers a novel strategy for improving the efficacy of ALA-PDT through the modulation of iron metabolism, achieved by targeting DMT1 and utilizing the iron chelator DFO. Additionally, DFO exhibited a dual mechanism, depending on cellular iron homeostasis.

Hormonal replacement therapy was not initiated due to the potential risk of tumor recurrence, and follow-up imaging was scheduled every 6 months for the first 2 years and then annually. No recurrence was observed at 24 months.

Furthermore, our work establishes SEC-ICP-MS as a sensitive and specific method for quantifying CuCOX and assessing mitochondrial metabolism. This platform holds promise for the identification of Cu-related biomarkers and therapeutic targets, particularly in the context of diseases such as renal cell carcinoma (RCC), where dysregulated Cu homeostasis plays a critical role.

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.