IREB2 (Iron Responsive Element Binding Protein 2)

Ultimately, seven key drug targets (SERPING1, TDRD9, GBAP1, FAM241A, ZKSCAN4, ZKSCAN3, Z94721.1) were consistently identified across two MR studies and validated. These targets offer new avenues for LC treatment, highlighting their potential in therapeutic development.

CIC, IREB2, POGZ, and PCDHG cluster are associated with neurodevelopmental disorders, supporting shared developmental mechanisms. Findings warrant investigation of pathways linking congenital anomalies and childhood cancer.

Single-cell transcriptomic analysis and in vitro knockdown experiments confirmed IREB2's role in modulating B-cell activation and apoptosis pathways within tumors. These results support COPD as an independent lung cancer risk factor and implicate IREB2 and CD27⁺ B cells in COPD-to-cancer progression, laying groundwork for early detection and targeted intervention in high-risk individuals.

Combining oxaliplatin with ferroptosis inducer Erastin enhanced cell death, reversed by ferroptosis inhibitor Ferrostatin-1. Our findings demonstrate that targeting FBXL5 disrupts iron homeostasis, triggers ferroptosis, and overcomes oxaliplatin resistance in CRC.

Given the complexity of glioblastoma, personalized ferroptosis-based approaches that address tumor heterogeneity, immune interactions, and metabolic adaptations are crucial for overcoming therapy resistance. Refining ferroptosis-targeted strategies by incorporating metabolic, immune, and genetic considerations can lead to more durable and effective therapies, ultimately transforming glioblastoma treatment and improving patient outcomes.

In addition, high-dose IR exposure can block NPC cells in the G2/M phase. Moreover, we found that the expression levels of three ferroptosis driver genes were lower in radioresistant NPC cell line High dose IR can induce ferroptosis in NPC cells, highlighting the potential for developing novel ferroptosis-based targets and overcoming radioresistance in clinical NPC treatments.

ZBTB7B exhibited a positive mediating effect in the association between lung cancer and HF risk (OR = 1.04; 95% CI 1.01-1.07; P < 0.05). This study highlights IREB2, KRTCAP2, MTX1P1, and ZBTB7B as potential therapeutic targets for cancer-related CVD risk, emphasizing the importance of considering genetic factors in understanding and managing cardiovascular complications associated with lung cancer.

Furthermore, we demonstrated that STK17B indirectly maintains activating phosphorylation of STAT3, a ferroptosis suppressor and a major driver of MM pathobiology. Our findings uncovered a clinically relevant and targetable STK17B-pIREB2S157/pHSPB1S15 signaling axis that suppresses ferroptosis and contributes to drug resistance in MM.

This study identifies IREB2 as a critical factor in the molecular mechanisms by which smoking accelerates facial aging, while also contributing to tumor development and immune evasion. Further functional exploration of IREB2 could uncover new therapeutic avenues to address these interconnected conditions.

GSVA and GSEA highlighted the involvement of TME-related pathways, such as transforming growth factor beta (TGF-β) and mechanistic target of rapamycin (mTOR) signaling pathways...The in vitro experiment on the key genes showed a consistent result with the bioinformatics finding. Our study provides insights into the prognostic biomarkers and molecular mechanisms in BRCA, offering potential therapeutic avenues and guiding personalized treatment strategies for improved patient outcomes.

In summary, we conducted a multi-omic studies, which integrated three levels to investigate the novel targets for LC. Through a series of verifications, RNASET2 was identified as the key gene for LC in the current research.

Blocking the TLR4/NF-κB cascade reversed the promoting effect of IREB2 on steatosis and inflammatory response. NAFLD treatment and prevention could benefit from IREB2, which may be closely related to TLR4/NF-κB signaling in lipid metabolism and glucose tolerance.