Early Growth Response Protein-1 Involves in Transforming Growth factor-β1 Induced Epithelial-Mesenchymal Transition and Inhibits Migration of Non-Small-Cell Lung Cancer Cells

Abstract

The zinc finger transcription factor EGR1 has a role in controlling synaptic plasticity, wound repair, femalereproductive capacity, inflammation, growth control, apoptosis and tumor progression. Recent studies mainlyfocused on its role in growth control and apoptosis, however, little is known about its role in epithelial-mesenchymaltransition (EMT). Here, we aim to explore whether EGR 1 is involved in TGF-β1-induced EMT in non-smallcelllung cancer cells. Transforming growth factor (TGF)-β1 was utilized to induce EMT in this study. Westernblotting, RT-PCR, and transwell chambers were used to identify phenotype changes. Western blotting was alsoused to observe changes of the expression of EGR 1. The lentivirus-mediated EGR 1 vector was used to increaseEGR1 expression. We investigated the change of migration to evaluate the effect of EGR 1 on non-small-celllung cancer cells migration by transwell chambers. After stimulating with TGF-β1, almost all A549 cells andLuca 1 cells (Non-small-cell lung cancer primary cells) changed to mesenchymal phenotype and acquired moremigration capabilities. These cells also had lower EGR 1 protein expression. Overexpression of EGR 1 gene withEGR 1 vector could decrease tumor cell migration capabilities significantly after adding TGF-β1. These datas howed an important role of EGR 1 in the EMT of non-small-cell lung cancer cells, as well as migration.