EGR1 (Early Growth Response 1)

In conclusion, our study reveals that ADE induces ferroptosis in HNSCC via the EGR1-ACSL4 axis. This finding highlights the potential of ADE as a therapeutic agent, and provides a mechanistic foundation for its future clinical applications in HNSCC.

NAT10 knockdown suppresses GSC proliferation and maintenance in vitro and attenuates tumor growth in vivo. Pharmacological inhibition of NAT10/ac4C-modified R-loops using remodelin phenocopies NAT10 genetic targeting, demonstrating therapeutic promise for targeting cancer.

The stability of RREB1 mRNA was assessed via Actinomycin D. Binding of RBM15 or insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) to RREB1, and EGR1 to RBM15 was confirmed by RIP and ChIP assay, respectively...This study confirmed that EGR1 activated RBM15 transcription, which mediated the m6A modification of RREB1 mRNA by recruiting IGF2BP2, thereby promoting malignant progression in gastric cancer. The discovery of this pathway provides a new perspective for revealing the pathogenesis of gastric cancer.

A BAG3-associated risk score derived from a 10-gene signature remained an independent prognostic factor for overall survival after clinical adjustment. These findings characterize a BAG3-associated TAM program with spatial, immunoregulatory, and prognostic relevance in HCC, and support its further evaluation in biomarker and mechanistic studies.

Treatment with Mithramycin A, a compound that disrupts EGR1-DNA interactions, dissolves NAB2::STAT6 condensates and reverses their aberrant gene expression and chromatin binding signatures. Our findings uncover a previously unrecognized role for NAB2::STAT6 in condensate-mediated oncogenic signaling and provide a mechanistic rationale for condensate-targeted therapy in SFT.

Based on these conclusions, we propose a refined model for predicting Snail target genes. Finally, given that inhibiting the Snail-EMT axis presents a plausible opportunity to limit cancer progression and improve patient outcomes, we also discuss clinically relevant pharmacological strategies for targeting Snail.

The present review outlines the context‑dependent regulatory effects of DYRK1A in CVDs, which are either protective or pathogenic depending on the disease type and stage. In addition, it emphasizes the requirement for further mechanistic evaluation and the development of DYRK1A‑targeted strategies to advance the translational of DYRK1A as a disease‑specific therapeutic target in CVDs.

These data indicate that Caspase14 promotes survival, proliferation, and metabolic reprogramming in resistant MCF7 cells via the EGR1/HIF-1α pathway. Our findings reveal a mechanistic link between Caspase14 and endocrine therapy resistance and nominate Caspase14 as a therapeutic target to overcome tamoxifen resistance, with potential translational relevance.

The EGR1-ZNF768-SLC7A11 axis constitutes a critical adaptive shield limiting lenvatinib efficacy in HCC. ZNF768 serves as a predictive biomarker and a high-value therapeutic target. Disrupting this axis offers a rational strategy to overcome therapeutic resistance and maximize the clinical potential of lenvatinib.

Collectively, our findings demonstrate that CEP72 functions as a key negative regulator of inflammation-driven hepatic fibrosis. CEP72 deficiency accelerates the progression of liver fibrosis through the EGR1-TNF-α signaling pathway. This study identifies a previously unrecognized protective role of CEP72 in hepatic fibrosis and highlights its potential as a novel therapeutic target for the treatment of S. japonicum-induced and other types of inflammation-associated liver fibrosis.

Interleukin-6 receptor inhibitors (e.g., tocilizumab) show robust efficacy in GCA but with notable non-responders; the JAK inhibitor upadacitinib demonstrated efficacy in a Phase III study, whereas IL-17 blockade (secukinumab) yielded inconsistent results...Mavrilimumab (GM-CSF receptor blockade) is promising in GCA. Recent studies have increasingly focused on short-term glucocorticoid therapy in combination with biologic agents. Advances in biomarker research, including investigation of the IL-6 receptor and IL-17A gene polymorphisms, may enable more targeted therapeutic strategies.

Immune differentiation analysis showed patients with NRF2High tumors enriched with CD68 have lower survival (p = 0.038) than those with CD68Low tumors, whereas NRF2Low tumors enriched with immune-activated markers such as CD3E and CD80 exhibit a better prognosis. This study is the first that shows classification of HGSOC based on NRF2 levels, highlights new biomarkers, and suggests IHC-labeling and genomic evaluation of NRF2 and immune markers for better prognosis.