Mobile website
Archive > Volume 22 Issue 5 > 2015,22(5):558-565. DOI:10.3872/j.issn.1007-385X.2015.05.002 Prev Next
Prompt Report
Roles of focal adhesion kinase in vascular endothelial cell proliferation, migration, apoptosis, and capilary-like structures formation
- Article
- Figures
- Metrics
- Preview PDF
- Reference
- Related
- Cited by
- Materials
Abstract:
Objective:To investigate roles for focal adhesion kinase (FAK) in the regulation of proliferation, migration, apoptosis, and angiogenesis of human vascular endothelial cells. Methods: Human umbilical vein endothelial cells (HUVECs) were transfected with FAK siRNA or treated with TAE226. FAK mRNA abundance in siRNA-transfected or TAE226-treated HUVECs and malignant pleural mesothelioma cell lines Y-MESO14 and NCI-H290 was determined by Real-time PCR. FAK protein was assessed by Western blotting, cell viability by MTT, apoptosis by flow cytometry, migration by Transwell assay, and capillary structure formation by matrigel-based tube formation assay in control, TAE-treated and FAK siRNA-transfected HUVECs. Results: FAK mRNA was significantly more abundant in HUVECs than in both Y-MESO-14 and NCI-H290 cell lines(P<0.05). rhVEGF treatment significantly increased FAK and pFAK protein levels of HUVECs (P<0.05). FAK siRNA effectively silenced FAK gene expression in the presence of rhVEGF in HUVECs (P<0.01). TAE226 at all concentrations used and FAK mRNA significantly inhibited proliferation, migration, and apoptosis of HUVECs (P<0.01). While rhVEGF significantly promoted angiogenesis, TAE226 and FAK siRNA significantly inhibited capillary structure formation in HUVECs (P<0.01). Conclusion: FAK siRNA plays important regulatory roles in vascular endothelial cell proliferation, migration, apoptosis, and capillary structure formation, and thus offer a novel target for angiogenesis-based cancer therapy.
Keywords:
Project Supported:
Project supported by the National Natural Science Foundation of China（No.81360350）
Clc Number:
