EGR1 (Early Growth Response 1)

Understanding EGR1's cell type-specific functions at the various levels will be helpful in understanding the normal development and in finding therapeutic targets in reproduction, cancer, and immune-related diseases. In this review, we briefly summarize the genetic anatomy with the molecular and developmental roles of EGR1.

This study demonstrates evidence for EBV particle exposure to influence microglial immune phenotypes by suppressing IFN production, providing a putative mechanism for EBV virion expression in the CNS to suppress anti-tumoral immunity against EBV+ cancers. These results are particularly relevant to the etiology of EBV+ primary CNS cancers in immunocompromised people, where microglial play a heightened role in protecting the CNS in the absence of adaptive immunity.

After eight years and treatment with lenalidomide with excellent clinical response, she developed progressive cytopenias and transformation to acute myeloid leukemia, myelodysplasia-related (AML-MR)...The patient was treated with combination azacitidine and venetoclax and an investigational immunotherapy within a clinical trial...Our findings expand the spectrum of dmin-associated oncogenic amplifications in myeloid neoplasms and highlight FLI1 and ETS1 as recurrent targets of 11q24-derived ecDNA amplification. Recognition of such rare events underscores the importance of integrative cytogenomic profiling for uncovering novel mechanisms of leukemic transformation and potential therapeutic targets.

We defined a novel ISG signature in iCCA and identified EGR1 as a critical driver of senescent tumor cells in iCCA.These findings offer new insights into senescent tumor cells and the immunosuppressive microenvironment.

This study reveals distinct molecular pathologies in the periarticular muscle of RA and OA. RA muscle shows an intense inflammatory profile potentially linked to cachexia, whereas OA muscle displays features of metabolic disease and pro-fibrotic remodelling.

This review systematically summarizes the molecular mechanisms underlying PD-L1 nuclear translocation, its biological functions, roles within the tumor microenvironment, and potential as a biomarker and therapeutic target. Emphasis is placed on addressing functional heterogeneity and mitigating experimental artifacts, which is critical for translational research.

These findings may facilitate the development of traditional medicinebased therapeutic strategies and provide insights for potential lead optimization in breast cancer drug discovery.

ALK mutations drive tumor stemness and drug resistance by blocking epithelial cell differentiation, activating CEACAM6-mediated signaling, enhancing chromatin accessibility, and remodeling the EGR1/PRC regulatory network. Targeting CEACAM6 and its downstream effector EGR1 may represent an effective strategy to overcome ALK-TKI resistance.

Disruption of EGR1 phase separation significantly alleviated cyst growth in the forskolin-induced 3D spheroid model of mIMCD3 cells and MDCK cyst model. These findings demonstrate that phase separation-mediated EGR1 condensates facilitate renal cyst development in ADPKD.

Melanoma A375 (vemurafenib [VEM]-sensitive) and A375R (VEM-resistant) cells were exposed to eIF4Fi RocA at varying doses and durations in vitro...Combined CR-1-31-B, EZH2i, and AKT1i effectively overcame resistance to RocA and VEM resistance both in vitro and in vivo. The eIF4F complex inhibitor reactivates ERK1/2-EZH2 and AKT1 signaling pathways, resulting in resistance to both eIF4Fi and VEM. Combined administration of an eIF4Fi with EZH2 and AKT1 inhibitors effectively enhances sensitivity to both eIF4F complex and BRAF inhibitors.

Pharmacological inhibition or genetic knockout of Padi2 attenuated silica-induced lung inflammation and fibrosis. These findings suggest that targeting PADI2 may represent a novel therapeutic strategy of silicosis.