Tumor Cell Invasion
|
0.100 |
PosttranslationalModification
|
phenotype |
BEFREE |
The secreted VEGFA from HCC cells activates phosphorylation of VEGFR2 to promotes tube formation, cell migration, and invasion of vascular endothelial cells <i>in vitro</i>, and promotes tumor growth and angiogenesis <i>in vivo</i>.
|
31799179 |
2019 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
When overexpressed in gastric cancer cells, VEGFR2 increased cellular proliferation and invasion in vitro and tumor formation in xenograft models.
|
30819137 |
2019 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Surprisingly, although there was no induction of intratumor hypoxia by anti-Sema4D therapy, the increase in local invasion and distant metastases was comparable with the one produced by VEGFR inhibition.
|
31239269 |
2019 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
While VEGF‑A binds to both VEGFR‑1 and VEGFR‑2, PlGF interacts exclusively with VEGFR‑1 triggering a signaling pathway involved in: i) tumor‑associated angiogenesis; ii) chemotaxis and invasion of the extracellular matrix (ECM) by cancer cells; and iii) mobilization of bone marrow‑derived myeloid cells that generate tumor‑associated macrophages.
|
29512738 |
2018 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Transwell assays reveals that VEGFR2 inhibition attenuates migration and invasion of osteosarcoma cells.
|
29225166 |
2018 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Furthermore, compared with shell/core-U118 (U) hydrogel microfibers, the expressions of matrix metalloproteinase-2 (MMP2), MMP9, vascular endothelial growth factor receptor-2 (VEGFR2) and O6-methylguanine-DNA methyltransferase (MGMT) which are related to tumor invasion and drug resistance were significantly enhanced in G/U hydrogel microfibers.
|
30048904 |
2018 |
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
In addition, ZEB1 shRNA inhibited the invasion of MDA‑MB‑231 cells and suppressed the expression of fetal liver kinase 1 (flk‑1).
|
29512767 |
2018 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Apatinib inhibit VEGF-mediated cell migration and invasion in CCA cell lines via inhibiting the VEGFR2/RAF/MEK/ERK and PI3K/AKT pathways.
|
30400838 |
2018 |
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Notably, results suggested that the downregulated VEGF‑A and VEGFR‑2 in TBMS1‑treated NCI‑H1299 cells were upregulated after inhibiting miR‑126‑5p, and overexpression of VEGF‑A or VEGFR‑2 could significantly reduce apoptosis and promote the migration and invasion of TBMS1‑treated NCI‑H1299 cells.
|
29363720 |
2018 |
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Compared with the high expression of miRNA‑195 in AMC‑HN‑8 cells, the expression levels of vascular endothelial growth factor receptor‑II protein and downstream signaling pathway proteins, which were associated with cell viability, migration, invasion and apoptosis, were markedly decreased compared with control or miRNA‑195 negative control treatment group.
|
29393451 |
2018 |
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Lactate, in turn, controlled VEGF-A/VEGFR2 expression and the resulting cell invasion.
|
29904943 |
2018 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
NHERF1 in turn inhibited the activation of VEGFR2 signaling which could be regulated by the interaction between NHERF1 and VEGFR2, resulting in the reduction of migration and invasion of colon cancer cells.
|
27999191 |
2017 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Polymer NPs with nM affinity to a key vascular endothelial growth factor (VEGF<sub>165</sub>) inhibit binding of the signalling protein to its receptor VEGFR-2, preventing receptor phosphorylation and downstream VEGF<sub>165</sub>-dependent endothelial cell migration and invasion into the extracellular matrix.
|
28644480 |
2017 |
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
The depth of interstitial and endovascular intrauterine trophoblast invasion and the immunohistochemical expression of vascular endothelial growth factor (VEGF), fetal liver kinase 1 (Flk1), interferon (IFN)-γ, migration inhibitory factor (MIF), and inducible nitric oxide synthase (iNOS; also known as nitric oxide synthase (NOS) 2) were evaluated.
|
27737730 |
2017 |
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
NVP-BEP800 down-regulated VEGFRs expression to significantly reduce tubular differentiation, as well as endothelial cell proliferation, migration, and invasion.
|
28359326 |
2017 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Triple combination of amiRNAs to VEGFRs reduced cell proliferation, increased apoptosis, and reduced cell migration and invasion in pancreatic cancer cell lines.
|
27889393 |
2017 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Eriocalyxin B also suppressed the expression of proliferation‑associated protein (proliferating cell nuclear antigen) and angiogenesis‑associated proteins (vascular endothelial growth factor and vascular endothelial growth factor receptor 2), as well as that of migration- and invasion‑associated proteins (matrix metalloproteinase 2 and 9).
|
26795301 |
2016 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
(2) VEGFR2 knockdown inhibited proliferation (P < 0.05), migration (P < 0.05), and invasion (P < 0.05) in Calu-1 cells.
|
26459253 |
2016 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Moreover, using the VEGFR2 inhibitor SU5416 and the VEGF-A neutralizing antibody to block VEGF-A/VEGFR2 signaling, our results suggested that tumor cell-derived VEGF-A promoted medulloblastoma cell migration and invasion through VEGFR2 signaling, and that both VEGF-A and VEGFR2 were required for the promoting effects of PERK activation on medulloblastoma cell migration and invasion.
|
25794107 |
2015 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Through its balanced inhibitory potency versus MET, TIE2, and VEGFR2, altiratinib provides an agent that inhibits three major evasive (re)vascularization and resistance pathways (HGF, ANG, and VEGF) and blocks tumor invasion and metastasis.
|
26285778 |
2015 |
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Inhibition of Gab1 and VEGFR-2 expression also caused decreased cell proliferation, cell cycle arrested in G1 phase, increased apoptosis, and decreased invasion in RBE cells.
|
26014518 |
2015 |
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
To determine the relationship of wnt proteins with invasion related protein, we also analyzed the association between wnt protein expression and the expression of matrix metalloproteinase-9 (MMP-9) and vascular endothelial growth factor receptor-2 (VEGFR-2).
|
24564183 |
2014 |
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Thus, components of the Rb-E2F pathway have been shown to regulate the expression of genes involved in angiogenesis, including VEGF and VEGFR, genes involved in epithelial-mesenchymal transition including E-cadherin and ZEB proteins, and genes involved in invasion and migration like matrix metalloproteinases.
|
24889531 |
2014 |
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
In addition, treatment with an NF-κB pathway activation inhibitor, at 10 μM, significantly decreased LPA-induced VEGF(121), VEGF(165) and VEGFR-2 mRNA expression and VEGF secretion, as well as LPA-induced SKOV3 invasion (p<0.05).
|
21782227 |
2011 |
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
GEP100-Arf6-AMAP1-cortactin pathway frequently used in cancer invasion is activated by VEGFR2 to promote angiogenesis.
|
21858086 |
2011 |