EGR1 (Early Growth Response 1)

Critically, both the CEP20-S46A mutation and CCDC116 knockdown abolished centrosomal localization and CA induction. These findings establish exogenous CML as a direct inducer of organelle-level carcinogenesis and provide molecular targets for developing food safety interventions against thermally processed food toxicity.

An EGR1+ neutrophil transcriptional signature predicted poor clinical outcomes across multiple cancer types. These findings identify EGR1 as a hypoxia-inducible driver of neutrophil-mediated immunosuppression and provide a basis for targeting the hypoxia-EGR1 axis to overcome immunotherapy resistance.

In vivo studies showed that lipid nanoparticle-delivered circular DNAzymes targeting the early growth response protein 1 (EGR1) mRNA achieved localized tumor suppression upon NIR irradiation, while exhibiting minimal gene silencing activity in normal organs. Our work establishes a versatile and effective platform for the spatiotemporal control of oligonucleotide functions in vivo, providing a powerful tool for the basic study of gene function and highlighting their potential in the development of safe and on-demand gene therapeutics.

This study establishes UBE2M as a critical tumor suppressor in melanoma through the MKK7 neddylation-JNK-EGR1 axis and highlights its potential as a therapeutic target.

This study reveals a noncanonical role for EGR1 mRNA as an epigenetic regulator of mitophagy in HCC, thus expanding the functional repertoire of mRNA molecules beyond protein coding. Targeting this noncanonical EGR1 ntmRNA-BNIP3 homodimerization mechanism may suggest new therapeutic strategies for treating HCC.

Our study provides initial evidence that PD-L1 might form HMGA1- and SMAD3-dependent complexes to bind the GAS6, EGR1 and CD274 promoters, thus modulating the transcription of GAS6, EGR1 and PD-L1 mRNA in cancer and sarcoma cells.

This research highlights the pivotal role of TOE1 in HCC, indicating its promise as a novel target for early detection, therapeutic strategies, immunological intervention, and prognosis assessment in HCC. These findings provide fresh perspectives for precision medicine in the context of HCC.

The HCC cells HepG2 and SNU449 were treated with five drugs, namely, dimethyl sulfoxide, AZ-628, SU-5402, TG-101209, and SPP-86, combined with donafenib to determine half-maximal inhibitory concentration values...Ferrous ion (Fe2+) and reactive oxygen species levels were measured after Erastin/RSL3 induction...In vivo experiments demonstrated a combined anti-tumor efficacy of AZ-628 and donafenib in HCC models (P < 0.0001). The findings of this study reveal a new combination therapy targeting the TK pathway for the treatment of HCC and provide a theoretical foundation for addressing donafenib resistance.

In addition, EV71 infection reduces cellular GSH and GPX4 expression, promotes ROS production, and decreases cell viability. These findings reveal significant transcriptional reprogramming of ferroptosis-associated genes during EV71 infection, highlighting a potential role for this pathway that requires direct experimental validation.

Together, these findings reveal a novel mechanism where Riluzole promotes apoptosis through upregulation of EGR1 , which then cooperates with YAP/p73 to activate Bax expression. These insights establish Riluzole as a promising therapeutic intervention for OS treatment through modulation of the EGR1 /Yap/p73/Bax signaling axis.

This study identified and validated prognostic biomarkers in HCC that effectively predict patient survival rates and immune infiltration characteristics. These findings provide a potential foundation for precision medicine strategies in HCC, offering novel insights into the tumor-immune microenvironment and its clinical implications.