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Resistance Mechanisms of Tumor Cells
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
In the hematopoietic system, other proteins are also able to exhibit these features. The EGR1 transcription factor (as well as EGR2 or EGR3) allows stem cells to go into homeostasis or dormancy to maintain them (Min et al., 2008; reviewed in Kühn et al., 2016). EGR1 has initially identified as activator of p21 and as gatekeeper of the TP53 (Krones-Herzig et al., 2003). Cells (over)expressing EGR1 protein can potentially escape treatment, and are presumably one of the reasons for relapses. A dormant cell needs only to switch back from this dormant state to the normal growth program. Recently, it has been shown that CDK4 but mainly overexpressed CDK6 (under certain stress conditions) re-activates dormant stem cells and causes tumor cell formation (Scheicher et al., 2015). Similarly, other factors have been described, such as HOXB4 (an OCT4 and GATA2 downstream target gene; Huang et al., 2016), which is capable of inducing sufficient amounts of the RUNX1 transcription factor to maintain hematopoietic stem cells (Teichweyde et al., 2017).
Proto-Oncogene and Onco-Suppressor Gene Expression
Published in Enrique Pimentel, Handbook of Growth Factors, 2017
The egr-1 gene encodes two distinct proteins of 82 and 88 kDa, depending on the site of initiation at an AUG or non-AUG codon.303 The two Egr-1 proteins bind to DNA in a sequence-specific manner, and this binding results in the activation of transcription. The single human egr-\ gene is located on chromosome region 5q23-q31.
Treatment of Vulnerable Plaques: Current and Future Strategies
Published in Levon Michael Khachigian, High-Risk Atherosclerotic Plaques, 2004
Leonard Kritharides, David Brieger, S. Benedict Freedman, Harry C. Lowe
Statins reduce early growth response gene product (Egr-1) expression in atherosclerotic plaques in apolipoprotein E knockout (apoE KO) mice.111 Egr-1 is important for the expression of platelet-derived growth factor (PDGF) which is critical for cellular migration in atherosclerotic lesions, local expression of which is stimulated by stimulation of the angiotensin II receptor121,122 (see gene therapy section below). Statins also inhibit angiotensin II-mediated signal transduction via modulating transcription factors c-jun and c-fos123 and inhibit PDGF-BB-mediated smooth muscle cell (SMC) migration and proliferation.124,125 Given the role of the angiotensin II receptor in atherosclerotic lesion progression and in generation of reactive oxygen species, inhibition of downstream effects of angiotensin-II activation may be important for inhibition of proliferative, oxidative, and inflammatory components of atherosclerotic lesion development.
Sex-dependent correlation between survival and expression of genes related to the circadian oscillator in patients with colorectal cancer
Published in Chronobiology International, 2018
Kristina Hasakova, Marian Vician, Richard Reis, Michal Zeman, Iveta Herichova
Early growth response protein 1 is involved in the cell cycle control, proliferation and apoptosis. Previously, protein and mRNA of egr1 was found increased in colorectal cancer tissue compared to paired normal mucosa. Positive expression of egr1 was significantly associated with age, lymph node and distant metastasis, tumor stage and poor survival (Myung et al. 2014). Tumor promoting role in colorectal cancer also supports a study which revealed that egr1 negatively regulated the apoptosis in HCT15 colon carcinoma cells (Mahalingam et al. 2010). In our study we observed a trend to increased egr1 expression in tumor compared to adjacent tissue in men and in women without distant metastases. According to our data, egr1 expression was decreased in tumor tissue of female patients with distant metastasis. Better survival rate in female patients was associated with high egr1 expression. On the other hand, male patients exhibited strong trend to better 5 year survival with low egr1 expression. Obviously egr1 plays a role in tumor progression regulation but the mechanism behind is not completely elucidated yet.
Identification of the potential targets for keloid and hypertrophic scar prevention
Published in Journal of Dermatological Treatment, 2018
Lianbo Zhang, Haiyan Qin, Zhuoxia Wu, Wanying Chen, Guang Zhang
Furthermore, EGR1 (connective degree = 21) was another significant node in PPI network and a significant TF in modules. EGR-1, early growth response protein-1, is a critical regulator in cell growth, differentiation and survival (30). Egr-1 has been found to be highly expressed in tissue of patients with scleroderma and has been proposed to be involved in tissue repair and fibrosis (30). Previous evidence has shown that the expression of EGR-1 in skin fibroblasts is closely associated with migration and myofibroblast transdifferentiation (31). The expression of EGR-1 is induced by tissue response to acute injury (32). The aberrant expression of EGR-1 is related with various diseases, such as inflammatory bowel disease (33), pulmonary disease (34), and atherosclerosis (35). EGR-1 has been proposed to be a potential drug for wound healing and tissue repair (36). Furthermore, previous evidence indicates the co-regulated interaction between Egr-1 and c-fos in some tissues (37). Thus, we speculated that Egr-1 and c-fos were significant regulators in skin scar formation.
Endostatin in fibrosis and as a potential candidate of anti-fibrotic therapy
Published in Drug Delivery, 2021
Zequn Zhang, Xi Liu, Zhaolong Shen, Jun Quan, Changwei Lin, Xiaorong Li, Gui Hu
Human EGR-1 (early growth response 1) is located on chromosome 5q31 and encodes an 80 kDa DNA binding transcription factor. EGR-1 expression levels are low or undetectable in resting cells but are elevated by many extracellular stimuli. The EGR-1 consists of an activation domain, inhibition domain, and a DNA binding domain. DNA binding domain is comprised of three zinc fingers targeting GC-rich DNA sequences. EGR-1 modulates the expression of various growth factors, cytokines, and adhesion molecules, including TGF-β, bFGF (basic fibroblast growth factor), PDGF-A, PDGF-B, IL-2, TNF-α, M-CSF (macrophage colony-stimulating factor), ICAM-1 (intercellular adhesion molecule 1), and CD44, thereby modulating signal transduction (Bhattacharyya et al. 2011; Li et al. 2020).