Abstract
Snail1 plays an important role in epithelial to mesenchymal transition (EMT) during tumor metastasis; however, whether Snai1 potentiates the process of neoangiogenesis is completely unknown. In the present study, tube formation assay was used to evaluate neoangiogenesis in vitro. The expression of Snai1 and other pro-neoangiogenic factors was measured by quantitative real time PCR. Tumor derived endothelial cells (TDECs) were stimulated with fibroblast growth factor 1 (FGF1) or VEGF and formed more tubes compared with untreated, whereas cells treated with Sulforaphane had less tube formation. Silencing SNAI1 significantly attenuated tube formation accompanied by decreased CD31, CD34, and VWF expression in TDECs compared with control. In contrast, overexpression of Snai1 led to more CD31, CD34, and VWF expression and tube formation. To determine if the observed effects of SNAI1 on tube formation was a global phenomenon, the same assay was conducted in normal mesenchymal stem cells (MSCs). SNAI1 silencing did not have any effect on tube formation in MSCs. The expression of TIMP2, ENG, and HIF1A was up-regulated 3-fold or higher after silencing SNAI1, and ID1, VEGFA, PLG, LECT1, HPSE were shown down-regulated. Taken together, our study elucidates an important role of EMT inducer Snai1 in regulating tumor neoangiogenesis, suggesting a potential therapeutic target for overcoming tumor EMT.
Highlights
Epithelial to mesenchymal transition (EMT) is a fundamental process in which epithelial cells undergo morphological changes to highly motile mesenchymal cells
tumor derived endothelial cell (TDEC) were treated with fibroblast growth factor (FGF), VEGF, or Sulforaphane, and we found cells stimulated with FGF and VEGF formed more tubes than untreated, whereas Sulforaphane attenuated tube formation (Figure 1A–D)
Overexpression of Snai1 led to more CD31, CD34, and VWF expression and tube formation (Figures 1G,H & 2)
Summary
Epithelial to mesenchymal transition (EMT) is a fundamental process in which epithelial cells undergo morphological changes to highly motile mesenchymal cells. One of the major effector of EMTs is the zinc-finger factor Snai1 [3,4]. The gene encoding Snail 1, SNAI1, has been shown through extensive research work to be indispensable for cancer metastasis, largely due its direct role in inhibiting the epithelial cell marker, E-cadherin [5,6,7,8]. Little is known about the contribution of the EMT program to neoangiogenesis. The objective of the current study was to evaluate whether EMT inducers impact the process of neoangiogenesis. As one of the hallmarks in EMT and metastatic progression [3,4,5,6,7,9], Snai was investigated to determine its contribution to the process of neoangiogenesis
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