scholarly journals Expression of early growth response-1 in colorectal cancer and its relation to tumor cell proliferation and apoptosis

2013 ◽  
Vol 31 (2) ◽  
pp. 788-794 ◽  
Author(s):  
DAE-SEONG MYUNG ◽  
YOUNG-LAN PARK ◽  
NURI KIM ◽  
CHO-YUN CHUNG ◽  
HYUNG-CHUL PARK ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Tumor Cell ◽  
Growth Response ◽  
Early Growth ◽  
Tumor Cell Proliferation ◽  
Early Growth Response ◽  
Proliferation And Apoptosis ◽  
Early Growth Response 1

scholarly journals Prostaglandins induce early growth response 1 transcription factor mediated microsomal prostaglandin E2 synthase up-regulation for colorectal cancer progression

Oncotarget ◽  
2015 ◽  
Vol 6 (37) ◽  
pp. 39941-39959 ◽  
Author(s):  
Konstantinos Stamatakis ◽  
Marta Jimenez-Martinez ◽  
Alba Jimenez-Segovia ◽  
Isabel Chico-Calero ◽  
Elisa Conde ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Transcription Factor ◽  
Prostaglandin E2 ◽  
Cancer Progression ◽  
Growth Response ◽  
Early Growth ◽  
Early Growth Response ◽  
Colorectal Cancer Progression ◽  
Early Growth Response 1

scholarly journals Serine 26 in Early Growth Response‐1 Is Critical for Endothelial Proliferation, Migration, and Network Formation

2021 ◽  
Author(s):  
Fernando S. Santiago ◽  
Yue Li ◽  
Levon M. Khachigian
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Response ◽  
Network Formation ◽  
Early Growth ◽  
Endothelial Cell Proliferation ◽  
Vascular Endothelial ◽  
Early Growth Response ◽  
Early Growth Response 1

Background Vascular endothelial cell proliferation, migration, and network formation are key proangiogenic processes involving the prototypic immediate early gene product, Egr‐1 (early growth response‐1). Egr‐1 undergoes phosphorylation at a conserved Ser26 but its function is completely unknown in endothelial cells or any other cell type. Methods and Results A CRISPR/Cas9 strategy was used to introduce a homozygous Ser26>Ala mutation into endogenous Egr‐1 in human microvascular endothelial cells. In the course of generating mutant cells, we produced cells with homozygous deletion in Egr ‐1 caused by frameshift and premature termination. We found that Ser26 mutation in Egr‐1, or Egr‐1 deletion, perturbed endothelial cell proliferation in models of cell counting or real‐time growth using the xCELLigence System. We found that Ser26 mutation or Egr‐1 deletion ameliorated endothelial cell migration toward VEGF‐A 165 (vascular endothelial growth factor‐A) in a dual‐chamber model. On solubilized basement membrane preparations, Ser26 mutation or Egr‐1 deletion prevented endothelial network (or tubule) formation, an in vitro model of angiogenesis. Flow cytometry further revealed that Ser26 mutation or Egr‐1 deletion elevated early and late apoptosis. Finally, we demonstrated that Ser26 mutation or Egr‐1 deletion increased VE‐cadherin (vascular endothelial cadherin) expression, a regulator of endothelial adhesion and signaling, permeability, and angiogenesis. Conclusions These findings not only indicate that Egr‐1 is essential for endothelial cell proliferation, migration, and network formation, but also show that point mutation in Ser26 is sufficient to impair each of these processes and trigger apoptosis as effectively as the absence of Egr‐1. This highlights the importance of Ser26 in Egr‐1 for a range of proangiogenic processes.

Role of early growth response 1 in arteriogenesis: Impact on vascular cell proliferation and leukocyte recruitment in vivo

2012 ◽  
Vol 107 (03) ◽  
pp. 562-574 ◽  
Author(s):  
Tibor Ziegelhoeffer ◽  
Matthias Heil ◽  
Silvia Fischer ◽  
Borja Fernández ◽  
Wolfgang Schaper ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Femoral Artery ◽  
Growth Response ◽  
Early Growth ◽  
Leukocyte Recruitment ◽  
Artery Ligation ◽  
Vascular Cell ◽  
Early Growth Response ◽  
Early Growth Response 1

SummaryBased on previous findings that early growth response 1 (Egr-1) participates in leukocyte recruitment and cell proliferation in vitro, this study was designed to investigate its mode of action during arteriogenesis in vivo. In a model of peripheral arteriogenesis, Egr-1 was significantly upregulated in growing collaterals of wild-type (WT) mice, both on mRNA and protein level. Egr-1−/− mice demonstrated delayed arteriogenesis after femoral artery ligation. They further showed increased levels of monocytes and granulocytes in the circulation, but reduced levels in adductor muscles under baseline conditions. After femoral artery ligation, elevated numbers of macrophages were detected in the perivascular zone of collaterals in Egr-1−/− mice and mRNA of leukocyte recruitment mediators was upregulated. Other Egr family members (Egr-2 to -4) were significantly upregulated only in Egr-1−/− mice, suggesting a mechanism of counterbalancing Egr-1 deficiency. Moreover, splicing factor-1, downregulated in WT mice after femoral artery ligation in the process of increased vascular cell proliferation, was upregulated in Egr-1−/− mice. αSM-actin on the other hand, significantly downregulated in WT mice, showed no differential expression in Egr-1−/− mice. While cell cycle regulator cyclin E and cdc20 were upregulated in Egr-1−/− mice, cyclin D1 expression decreased below the detection limit in collaterals, and the proliferation marker ki67 was not differentially expressed. In conclusion, compensation for deficiency in Egr-1 function in leukocyte recruitment can presumably be mediated by other transcription factors; however, Egr-1 is indispensable for effective vascular cell cycle progression in arteriogenesis.

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