Egr-1 regulates the transcription of NGX6 gene through a Sp1/Egr-1 overlapping site in the promoter

Liu, Minji; Wang, Xiaoyan; Peng, Ya; Shen, Shourong; Li, Guiyuan

doi:10.1186/1471-2199-15-14

Cited by 11 publications

(13 citation statements)

References 15 publications

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“…EGR1 plays complex and often contradictory roles in human malignancies. 55,56 Based on previous reports, EGR1 also displays both facilitating and repressing effects in HCC. [26][27][28][29][30][31][32] For instance, EGR1 functions as an oncogene, promoting HCC growth and migration/invasion 27,29,31 and enhancing the drug resistance of HCC cells, likely through autophagy.…”

Section: Discussionmentioning

confidence: 82%

<p>CD24 isoform a promotes cell proliferation, migration and invasion and is downregulated by EGR1 in hepatocellular carcinoma</p>

Li¹,

Chen²,

Ge³

et al. 2019

OTT

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Introduction: CD24 is known as a heavily glycosylated cell surface molecule that is highly expressed in a wide variety of human malignancies. Previous studies have shown that CD24 plays an important role in self-renewal, proliferation, migration, invasion and drug resistance of hepatocellular carcinoma (HCC). However, little is known about the expression and function of CD24 isoform a (CD24A) and CD24 isoform b (CD24B) in HCC. Materials and methods: Quantitative real-time polymerase chain reaction (qPCR) and Western blotting were performed to detect CD24 and EGR1 expression in HCC cells and tissue. The function of CD24 in cell proliferation was verified with MTT assays, colony formation assays and tumor xenograft models. Wound healing assays and invasion assays were performed to clarify the function of CD24 in the regulation of cell migration and invasion in HCC. A dual luciferase reporter assay and chromatin immunoprecipitation assay were used to analyze the regulation mechanism of CD24A. Results: CD24A but not CD24B, which was barely detected by qPCR and Western blotting, is significantly upregulated in HCC tissue. Both CD24A and CD24B contribute to HCC cell proliferation, migration and invasion, but CD24A is more effective than CD24B. EGR1 downregulates CD24A and exerts transcription-promoting activity on the CD24A promoter. Furthermore, EGR1 represses HCC cell proliferation via downregulation of CD24A. Conclusion: CD24A is the predominant CD24 isoform in HCC and plays a major role in cell proliferation, migration, and invasion. EGR1 can exert its antitumor effect through transcriptional downregulation of CD24A in HCC.

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Section: Discussionmentioning

confidence: 82%

<p>CD24 isoform a promotes cell proliferation, migration and invasion and is downregulated by EGR1 in hepatocellular carcinoma</p>

Li¹,

Chen²,

Ge³

et al. 2019

OTT

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“…DNA methylation of promoter regions is associated with transcriptional silencing, either by preventing the binding of specific transcription factors or through the recruitment of methyl CpG binding proteins [ 25 ]. Egr-1 and SP1 are known to act as positive regulators of NKX6-2 ; this might elucidate the effect of these transcription factors on NKX6-2 gene [ 26 ]. IPA mapped this gene within the Wnt/ β -catenin and P38 MAPK signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

Reduced Representation Bisulfite Sequencing Determination of Distinctive DNA Hypermethylated Genes in the Progression to Colon Cancer in African Americans

Ashktorab

Shakoori

Zarnogi

et al. 2016

Gastroenterology Research and Practice

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Background and Aims. Many studies have focused on the determination of methylated targets in colorectal cancer. However, few analyzed the progressive methylation in the sequence from normal to adenoma and ultimately to malignant tumors. This is of utmost importance especially in populations such as African Americans who generally display aggressive tumors at diagnosis and for whom markers of early neoplasia are needed. We aimed to determine methylated targets in the path to colon cancer in African American patients using Reduced Representation Bisulfite Sequencing (RRBS). Methods. Genomic DNA was isolated from fresh frozen tissues of patients with different colon lesions: normal, a tubular adenoma, a tubulovillous adenoma, and five cancers. RRBS was performed on these DNA samples to identify hypermethylation. Alignment, mapping, and confirmed CpG methylation analyses were performed. Preferential hypermethylated pathways were determined using Ingenuity Pathway Analysis (IPA). Results. We identified hypermethylated CpG sites in the following genes: L3MBTL1, NKX6-2, PREX1, TRAF7, PRDM14, and NEFM with the number of CpG sites being 14, 17, 10, 16, 6, and 6, respectively, after pairwise analysis of normal versus adenoma, adenoma versus cancer, and normal versus cancer. IPA mapped the above-mentioned hypermethylated genes to the Wnt/β-catenin, PI3k/AKT, VEGF, and JAK/STAT3 signaling pathways. Conclusion. This work provides insight into novel differential CpGs hypermethylation sites in colorectal carcinogenesis. Functional analysis of the novel gene targets is needed to confirm their roles in their associated carcinogenic pathways.

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“…Underscoring our conclusions is the evidence of increased Egr-1 protein and mRNA expression during early stages of cysteamine-induced duodenal ulcer, while Egr-1 antisense oligonucleotide adminis tration caused the clinical picture of the condition to worsen [18]. According to publications, Egr-1 may act by binding to promoter regions of genes that are identical to that of another zinc-binding transcription factor Sp1 [13,19]. Regulatory activity of Egr-1 and Sp1, admittedly, may include both competition and complementation.…”

Section: Fig 3 Egr-1 Protein and Mrna Content In Rat Gastric Mucosamentioning

confidence: 65%

Redox-sensitive transcription factors EGR-1 and SP1 IN the pathogenesis of experimental gastric ulcer

Beregovyi¹,

Chervinska²,

Dranitsina³

et al. 2015

Ukr.Biochem.J.

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Changes in redox status of gastric mucosa cells are the main pathogenic factor of gastric erosion and gastric ulcer development. Pro-oxidants can affect cell transcription activity via changes in redox-sensitive transcription factors. Egr-1 and Sp-1 may regulate the transcription of genes that are associated with the pathogenesis of gastric ulcer (growth factors, cell cycle regulators, etc.). The aim of the present study was to reveal the possible involvement of zinc-finger transcription factors Egr-1 & Sp-1 in the molecular mechanisms underlying gastric lesions caused by aspirin administration and stress. Gastric ulcer was induced in male rats (180-220 g) by immobilization stress combined with water-immersion (IMO-WI) or aspirin gavage (10 mg/100 g). The rats were euthanized 20 min, 1 hour, or 3 hours following the ulcerogenic factor exposure. Protein expression was determined by Western blot analysis and RT-PCR; levels of SH-groups of proteins were determined by method of Ellman et al. Development of gastric ulcer lesions was associated with twofold (P < 0.05) decrease in concentration of protein SH-groups in the rat gastric mucosa. These changes were accompanied by significant (р < 0.05) increase in the expression of Egr-1 mRNA and protein in both gastric ulcer models, and the changes in IMO-WI were more profound. Increased levels of Egr-1 were associated with the decrease in Sp1 protein levels. We showed for the first time the competitive interaction between redoxsensitive transcription factors Egr-1 and Sp1 in the early phases of gastric ulcer development, which might facilitate inducible transcriptional activity of Egr-1 at the expense of reduction in Sp1 activity.

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Egr-1 regulates the transcription of NGX6 gene through a Sp1/Egr-1 overlapping site in the promoter

Cited by 11 publications

References 15 publications

<p>CD24 isoform a promotes cell proliferation, migration and invasion and is downregulated by EGR1 in hepatocellular carcinoma</p>

<p>CD24 isoform a promotes cell proliferation, migration and invasion and is downregulated by EGR1 in hepatocellular carcinoma</p>

Reduced Representation Bisulfite Sequencing Determination of Distinctive DNA Hypermethylated Genes in the Progression to Colon Cancer in African Americans

Redox-sensitive transcription factors EGR-1 and SP1 IN the pathogenesis of experimental gastric ulcer

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