Given that matrix metalloproteinases 9 (MMP9) and its associated vascular endothelial growth factor (VEGF) are critical for tumor vascularization and invasion under castration-resistant condition, it is therefore of great importance to define the functional association and interplay between androgen receptor (AR) and MMP9 and their associated key survival and invasion pathways in PCa cells.
Programmed death ligand-1 (PD-1/PD-L1), matrix metalloproteinases (MMPs), EpCAM (Trop1) and Trop2, cancer-testis antigen MAGE-A3, epidermal growth factor receptor (EGFR), folate receptor alpha (FRα), vascular endothelial growth factor (VEGF), and galectin-3 (Gal-3) have all been implicated as crucial factors involved with tumor survival and invasion.
In addition, the ternary complexes were able to downregulate both HIF-1α and VEGF expression in UM cells, and successfully inhibit UM migration and invasion.
Results indicated that icaritin can realize dosage-dependent inhibition of CNE2 cell proliferation, migration, and invasion and inhibit the expression levels of VEGF, KDR, bFGF, MMP2, and MMP9.
HIF-1α and VEGFA are the target genes of miR20b and miR20b downregulation activated HIF-1α-mediated VEGFA transcription and ASC-induced BC migration and invasion.
Downregulation of the miR-221/222 cluster diminished the invasion, migration, proliferation, and angiogenesis with reduced protein levels of matrix metalloproteinase-2 (MMP-2), MMP-9, and vascular endothelial growth factor in glioblastoma cells.
PAMSPF/p53/RG suppressed human umbilical vascular endothelial cells (HUVECs) migration, invasion and tube formation through decreasing the VEGF expression.
VEGFA played an important role in hypoxia-induced VM through regulating EMT and stemness, which may eventually fuel the migration and invasion of SACC.
The high expression of VEGF-A and VEGFR1 and associated immunosuppressive microenvironment were observed in NF-PitNETs with CS invasion, suggesting that a novel targeted therapy can be applied.
The expression of EGFR, VEGF, and MMP proteins was dramatically down-regulated, which may partially account for their inhibition of invasion and metastasis of CRC.
This study aimed to investigate how bevacizumab, a vascular endothelial growth factor A (VEGFA) neutralizing antibody applied in clinic, affects the tight junction protein CLDN5 and subsequently influences tumor cell invasion and potential metastasis.
Our results suggest that treatment of human umbilical vein endothelial cell (HUVECs) with didymin significantly prevented the VEGF-induced cell proliferation, migration, and invasion.
Transfection with piRNA-823 mimic or treatment with MM-derived-EVs significantly promoted the proliferation, tube formation, and invasion of EA.hy926 cells by enhancing the expression of VEGF, IL-6, and ICAM-1 and attenuating apoptosis.
In our study, we found that emodin inhibited the invasion and migration abilities of RKO cells and decreased the expression of matrix metalloproteinase-7 (MMP-7), MMP-9, and vascular endothelial growth factor (VEGF) in a dose-dependent manner.
Using the mutant form of the natural apelin-13 peptide, the authors showed reduction of both angiogenesis and invasion in the GBM models, and further increased the efficacy of anti-VEGF therapy.
VEGF is highly expressed in serum of patients with cholangiocarcinoma, it promotes angiogenesis, proliferation and invasion of gallbladder cancer cells, and inhibits apoptosis of tumor cells.
There was no difference observed in cell apoptosis rate; however, combined silencing of VEGF-A and Ang-2 resulted in a stronger inhibition of cell proliferation and invasion (<i>P</i><0.05).
Vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMPs) have been implicated in the invasion and metastasis of various malignant tumor types, such as lung cancer and gastric carcinoma.