EGR2 (Early Growth Response 2)

METTL3 enhances AFAP1-AS1 stability via m6A modification recognized by YTHDF2 and IGF2BP1, which subsequently increases EGR2 expression by improving its mRNA stability. EGR2 directly activates transcription of immune checkpoint and epithelial-mesenchymal transition (EMT)-related genes. This METTL3/AFAP1-AS1/EGR2 signaling axis drives PC malignancy and immune resistance, offering potential therapeutic targets for PC treatment.

Additionally, SLC16A3 downregulation reduced cisplatin sensitivity in LUAD cells. Our study highlights the clinical translational potential of a five-gene zinc homeostasis network signature in predicting prognosis and guiding personalized therapeutic strategies for LUAD.

These findings suggest LPXN may influence breast cancer progression through HDAC6/EGR2-mediated regulation of macrophage polarization. In conclusion, our study demonstrated that the LPXN/HDAC6/EGR2 axis promotes breast cancer progression by augmenting macrophage M2 polarization.

RNA-sequencing analysis showed that Egr2 enhanced myelination by inhibiting PDGFRα. Together, these results revealed that the Egr2/PDGFRα axis mediates distinct peer effects in rescuing SI-induced hypomyelination and social ability impairment.

While univariable analysis revealed shorter TTFT for Binet A patients with any ATM aberration compared to ATM-wildtype, multivariable analysis identified only del(11q), trisomy 12, SF3B1, and EGR2 mutations as independent prognosticators of shorter TTFT among Binet A patients and within M-CLL and U-CLL subgroups. These findings highlight del(11q), and not ATM mutations, as a key biomarker of increased risk of early progression and need for therapy, particularly in otherwise indolent M-CLL, providing insights into risk-stratification and therapeutic decision-making.

Finally, we introduced a virus overexpressing PDK4 and demonstrated that EGR2 could regulate the transcriptional level of PDK4 to affect the expression of IL-8, and ultimately alter the metastatic ability of hepatocellular carcinoma cells. Our study demonstrates that EGR2 may be a valuable target for future intervention in the disease process of hepatocellular carcinoma and refines the mechanism at the microscopic level of Tumor-associated macrophages.

The identification of EGR2 as a key SPRG and its functional impact on bladder cancer cells further highlights its significance in bladder cancer development and progression. Overall, SPRGS may serve as important prognostic markers and predictive biomarkers for bladder cancer patients, guiding treatment decisions and improving patient outcomes.

Taken together, FTO suppresses PCa progression by regulating EGR2 methylation. We uncovered a novel regulatory mechanism of FTO in PCa and provide a new potential therapeutic target for PCa.

NGS played a significant role in TTFT prognostic analysis, with mutations in EGR2 、 FBXW7 、 RPS15 associated with shorter TTFT. EGR2 serves as an independent predictor of poor outcome. Chronic lymphocytic leukemia

Finally, a refined EGR2 gene signature is a biomarker for type I interferon-associated CAR T-cell failure and shorter patient survival. These findings connect prolonged CAR T-cell activation with deleterious immunoinflammatory signaling and point to an EGR2-type I interferon axis as a therapeutically amenable biologic system.

Conclusively, temozolomide repressed glioblastoma progression by repressing the LINC00470/EGR2/SOX4 axis.