ArticleJournal of cellular and molecular medicine2019
EGR1 interacts with DNMT3L to inhibit the transcription of miR-195 and plays an anti-apoptotic role in the development of gastric cancer.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 62 citations in OpenAlex.
- Early growth response 1 promotes RNA polymerase I-directed transcription and cancer growth by activating RRN3 expression.Communications biology · 2026Article
- Dysregulated proliferation and immune response induced by estrogen in Egr1 knockout uterus are similar to those in immature uterus.BMC genomics · 2025Article
- DNMT3L inhibits hepatocellular carcinoma progression through DNA methylation of CDO1: insights from big data to basic research.Journal of translational medicine · 2024Article
- Review
- Lentinan induces apoptosis of mouse hepatocellular carcinoma cells through the EGR1/PTEN/AKT signaling axis.Oncology reports · 2023Article
- CNN2 silencing inhibits colorectal cancer development through promoting ubiquitination of EGR1.Life science alliance · 2023Article
- miR-let-7c-3p targeting on Egr-1 contributes to the committed differentiation of leukemia cells into monocyte/macrophages.Oncology letters · 2022Article
- Article
- METTL7B contributes to the malignant progression of glioblastoma by inhibiting EGR1 expression.Metabolic brain disease · 2022Article
- EGR1 Enhances Lymphangiogenesis via SOX18-Mediated Activation of JAK2/STAT3 Pathway.Computational and mathematical methods in medicine · 2022Article
- Molecular Characterization, Tumor Microenvironment Association, and Drug Susceptibility of DNA Methylation-Driven Genes in Renal Cell Carcinoma.Frontiers in cell and developmental biology · 2022Article
- NOL6 Regulates the Proliferation and Apoptosis of Gastric Cancer CellsFrontiers in oncology · 2022Article
- Article
- Effects of mir-195 Targeted Regulation of JAK2 on Proliferation, Invasion, and Apoptosis of Gastric Cancer Cells.Computational and mathematical methods in medicine · 2022Article
- The emerging potentials of lncRNA DRAIC in human cancers.Frontiers in oncology · 2022Review
- Integrated bioinformatical analysis, machine learning andFrontiers in pharmacology · 2022Article
- MicroRNAs as novel peripheral markers for suicidality in patients with major depressive disorder.Frontiers in psychiatry · 2022Article
- Oncogenic role of early growth response-1 in liver cancer through the regulation of the microRNA-675/sestrin 3 and the Wnt/β-catenin signaling pathway.Bioengineered · 2021Article
- Engineering an anti-HER2 biparatopic antibody with a multimodal mechanism of action.Nature communications · 2021Article
- CD105 expression is associated with invasive capacity in ovarian cancer and promotes invasiveness by inhibiting NDRG1 and regulating the epithelial-mesenchymal transition.American journal of translational research · 2021Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
EGR1 regulates the expression of its downstream target genes and may exert different biological effects in different tumours. We found that the expression of EGR1 was increased in gastric cancer (GC), and silencing the expression of EGR1 promoted the apoptosis of GC cells. Moreover, overexpression of EGR1 repressed the apoptosis of GC cells. Bioinformatics analysis showed that EGR1 had binding sites at the upstream promoter region of miR-195; ChIP assays were applied to determine EGR1 occupancy of the miR-195 promoter. The RT-PCR results showed that EGR1 suppressed the expression of miR-195. The mechanism by which EGR1 acts as a transcriptional repressor is still unclear. Bioinformatics analysis showed that EGR1 may interact with DNMT3L. We confirmed that EGR1 and DNMT3L formed a complex, and EGR1 was an important player in the transcriptional control of miR-195. Overexpression of miR-195 inhibited proliferation and promoted apoptosis in GC cells. We found a well-matched miR-195 binding site at the AKT3 3'-UTR. Double luciferase reporter assays showed that AKT3 was a target of miR-195, and silencing AKT3 repressed cell proliferation and promoted apoptosis. Our results indicated EGR1 may interact with DNMT3L to inhibit the miR-195-AKT3 axis and regulate the GC cell apoptosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.