AI Article Synopsis
- PAI-1 plays a crucial role in breast cancer by contributing to tumor growth and metastasis.
- EGF stimulates PAI-1 expression in MCF-7 breast cancer cells by activating the transcription factor Elk-1.
- Elk-1 binds to the PAI-1 promoter, and its phosphorylation, which is necessary for this binding, is dependent on EGF.
Article Abstract
PAI-1 (plasminogen activator inhibitor-1) in breast cancer cells is involved in tumour development and metastasis of breast cancer cells. PAI-1 function and the regulation of its expression have been precisely investigated. Here we report that EGF, which promotes breast cancer tumour growth and survival, rapidly induces PAI-1 expression in the breast adenocarcinoma cell line MCF-7 through the activation of the transcription factor Elk-1. We have found that the PAI-1 promoter fragment (-140 to +173) containing the Ets consensus binding site is activated by Elk-1. Chromatin immunoprecipitation analysis confirms in vivo binding of Elk-1 to the PAI-1 promoter and demonstrates that Elk-1 phosphorylation on the Ets binding site is EGF-dependent.
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| http://dx.doi.org/10.1016/j.bbagrm.2010.08.004 | DOI Listing |
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Article Synopsis
- PAI-1 plays a crucial role in breast cancer by contributing to tumor growth and metastasis.
- EGF stimulates PAI-1 expression in MCF-7 breast cancer cells by activating the transcription factor Elk-1.
- Elk-1 binds to the PAI-1 promoter, and its phosphorylation, which is necessary for this binding, is dependent on EGF.
Hemin upregulates Egr-1 expression in vascular smooth muscle cells via reactive oxygen species ERK-1/2-Elk-1 and NF-kappaB.
Circ Res
January 2008
Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, USA.
Reactive oxygen species (ROS) and oxidant stress are important mediators of cardiovascular pathologies including atherosclerosis. One source of ROS in the vasculature is free heme released from hemoglobin. Because Egr-1, the regulator of cell proliferation and apoptosis, is also induced by oxidant stress and is likewise implicated in atherosclerosis, we examined the regulation of Egr-1 by heme in vascular smooth muscle cells (SMCs).
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