Novel role of Snail 1 in promoting tumor neoangiogenesis

Autor: Yi-Kun Zhang, Yu-Wei Guo, Yang Yue, Hua Wang
Jazyk: angličtina
Rok vydání: 2019
Předmět:
0301 basic medicine
Inhibitor of Differentiation Protein 1
Vascular Endothelial Growth Factor A
Lung Neoplasms
Antigens
CD34
Fibroblast growth factor
Biochemistry
0302 clinical medicine
Isothiocyanates
RNA
Small Interfering
tumor derived endothelial cells
Lung
Research Articles
Neoangiogenesis
Glucuronidase
Tube formation
Neovascularization
Pathologic
Chemistry
Endoglin
epithelial to mesenchymal transition
Gene Expression Regulation
Neoplastic
Platelet Endothelial Cell Adhesion Molecule-1
Vascular endothelial growth factor A
Cell Transformation
Neoplastic
030220 oncology & carcinogenesis
Sulfoxides
Fibroblast Growth Factor 1
Intercellular Signaling Peptides and Proteins
Research Article
Signal Transduction
Epithelial-Mesenchymal Transition
Primary Cell Culture
Biophysics
03 medical and health sciences
von Willebrand Factor
Gene silencing
Anticarcinogenic Agents
Humans
Epithelial–mesenchymal transition
Molecular Biology
Tissue Inhibitor of Metalloproteinase-2
Mesenchymal stem cell
Endothelial Cells
Membrane Proteins
Mesenchymal Stem Cells
Cell Biology
Hypoxia-Inducible Factor 1
alpha Subunit
030104 developmental biology
HIF1A
SNAI1
Snai1
Cancer research
Snail Family Transcription Factors
Zdroj: Bioscience Reports
ISSN: 1573-4935
0144-8463
Popis: 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.
Databáze: OpenAIRE
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