EGR1 (Early Growth Response 1)

USP20 acts as a critical metabolic checkpoint that orchestrates CD8+ T cell exhaustion and therapeutic response. Targeting the USP20-cholesterol-autophagy axis represents a promising strategy to reverse immune suppression and unlock the full potential of KRASG12D inhibitors in PDAC.

EGR1 and PTGS2 are central nodes through which APM precipitates MASLD and accelerates progression to HCC. We propose a "dual-track" oncogenic paradigm: Track A follows the canonical MASLD-HCC axis (bile-acid retention - lipid deposition - TNF/IL-17-driven ROS-mutational amplification), whereas Track B allows APM, via PTGS2/EGR1, to usurp gate-keeper proteins governing proliferation and apoptosis, initiating malignant programming before overt steatosis develops. These findings provide mechanistic insight into APM-related hepatocarcinogenesis, nominate tractable diagnostic biomarkers and therapeutic targets, and inform future re-evaluation of APM carcinogenicity classifications.

The EGR1-driven GLUL/mTOR axis in PSCs suppresses pancreatic cancer progression by inhibiting PSC activation, reducing cancer cell macropinocytosis, and restraining metastasis. This axis represents a promising therapeutic target for disrupting PSC-cancer cell crosstalk in pancreatic cancer.

Abbreviations: AAV: adeno-associated virus; ACTB/β-actin: actin, beta; AIF1/IBA1: allograft inflammatory factor 1; BAF: bafilomycin A1; BNIP3: BCL2/adenovirus E1B interacting protein 3; CCI: controlled cortical impact; COX8: cytochrome c oxidase subunit 8; CUT&Tag: cleavage under targets and tagmentation; DAPI: 4,'6-diamidino-2-phenylindole; DEGs: differentially expressed genes; eGFP: enhanced green fluorescent protein; EGR1: early growth response 1; GFAP: glial fibrillary acidic protein; GO: gene ontology; GSEA: gene set enrichment analysis; HCQ: hydroxychloroquine; HIF1A/HIF-1α: hypoxia inducible factor 1, alpha subunit; IGV: integrative genomics viewer; KEGG: Kyoto encyclopedia of genes and genomes; KO: knockout; LAMP1: lysosomal-associated membrane protein 1; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; Lv: lentivirus; MAP2: microtubule-associated protein 2; mCherry: monomeric cherry fluorescent protein; mRFP: monomeric red fluorescent protein; MTOR: mechanistic target of rapamycin kinase; MUT: mutant; MWM: Morris water maze; NAB1: Ngfi-A binding protein 1; NAB2: Ngfi-A binding protein 2; RBFOX3/NeuN: RNA binding protein, fox-1 homolog (C. elegans) 3; OGD: oxygen-glucose deprivation; OLIG2: oligodendrocyte transcription factor 2; PBS: phosphate-buffered saline; PECAM1/CD31: platelet/endothelial cell adhesion molecule 1; PFA: paraformaldehyde; PPI: protein-protein interaction; Puro: puromycin; ROI: region of interest; ROS: reactive oxygen species; SEM: standard error of the mean; SQSTM1/p62: sequestosome 1; TBI: traumatic brain injury; TOMM20: translocase of outer mitochondrial membrane 20; TSA: tyramide signal amplification; TUNEL: terminal deoxynucleotidyl transferase dUTP nick end labeling; VDAC1: voltage-dependent anion channel 1; WT: wild-type.

Immunohistochemistry (IHC) validation further confirmed the elevated expression of SLC4A4 and H2AFJ in advanced-stage PCa. Overall, this study establishes an ST-based framework for predicting PCa progression and provides valuable insight for the identification of progression-associated genes holding promise as clinical biomarkers.

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.