Furthermore, the overexpression of miR‑206 notably suppressed the proliferation, migration and invasion of RCC cells, and these effects were enhanced by the knockdown of vascular endothelial growth factor (VEGF); cell growth and metastasis induced by miR‑206 inhibitors could be reversed by the knockdown of VEGF.
Calcineurin and its substrate, nuclear factor of activated T cells (NFAT), mediate the downstream signaling of VEGF, and is critical in the process endothelium activation and tumor metastasis.
Fifty tissue specimens were collected from gastric carcinoma with spinal metastasis and set as test group A; 30 tissue specimens of primary gastric carcinoma were collected and set as control group B; 30 healthy paracancerous gastric tissue specimens were collected and set as control group C. The expression levels of MMP-9 and vascular endothelial growth factor (VEGF) in the specimens were analyzed by immunohistochemistry.
β-Elemene also regulates the expression of several key molecules that are involved in tumor angiogenesis and metastasis including vascular endothelial growth factor (VEGF), matrix metalloproteinases (MMPs), E-cadherin, N-cadherin, and vimentin.
In addition, the expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF), which are known to be related to angiogenesis and metastasis, was also inhibited.
The long-period improvement of the tumor hostile environment downregulated the expression of hypoxia inducible factor (HIF)-1α and vascular endothelial growth factor (VEGF), further preventing tumor growth and metastasis.
Whereas wild-type p53 (wtp53) promotes cell-cycle arrest and apoptosis and inhibits vascular endothelial growth factor-dependent angiogenesis, mtp53 fails to regulate these functions, resulting in tumor vascularization, growth, resistance to chemotherapy, and metastasis.
The crucial role of VEGF receptor 2 (VEGFR2) signaling in the angiogenesis and metastasis of solid tumors has prompted the development of inhibitors with minimal bystander effects.
Adeno-associated virus 2 mediated gene transfer of vascular endothelial growth factor Trap (AAV2-VEGF-Trap) has been reported to inhibit the growth of primary tumor as well as distant metastasis in 4T1 metastatic breast cancer models.
We found survival benefits in patients treated with first-line vascular endothelial growth factor-tyrosine kinase inhibitors (VEGF-TKIs, first-line PFS, and total PFS, all P < 0.05), cytoreductive nephrectomy (CSS, P < 0.0001), metastasectomy (CSS, P = 0.0017), and patients with metachronous metastasis (first-line PFS, total PFS, and CSS, all P < 0.05).
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.
Moreover, using a dataset of breast cancer patients we show that the co-expression of HMGA1, FOXM1 and VEGFA is a negative prognostic factor of distant metastasis-free survival and relapse-free survival.
Whereas Wi-A binds to vimentin and heterogeneous nuclear ribonucleoprotein K (hnRNP-K) with high efficacy and downregulates its effector proteins, MMPs and VEGF, involved in cancer cell metastasis, 3βmWi-A was ineffective.
Additionally, we verified that miR-1249 suppressed CRC proliferation and angiogenesis by targeting VEGFA as well as inhibited CRC metastasis by targeting both VEGFA and HMGA2.
Collectively, our findings indicate that downregulation of miR20b by ASCs/SCF activates HIF-1α/VEGFA and induces BC cell EMT and metastasis, suggesting that this process is activated by the p-c-Kit/MAPK-p38/E2F1 pathway.
When the primary tumor showed Nrf2 gene mutation, the C/A or A/A genotype, or elevated Nrf2 protein expression, the response of metastases to vascular endothelial growth factor-targeting therapy was significantly worse (p = 0.0142, p = 0.0018, and p < 0.0001, respectively), and overall survival was significantly reduced (p = 0.0343, p = 0.0421, and p < 0.0001, respectively).
Strategies restoring miR-126-3p expression or targeting VEGF-A or ADAM9 could restrain growth and metastasis of dabrafenib-resistant melanomas and increase their drug sensitivity.
The present study aimed to determine whether BDNF, TrkB, VEGF and CD105 are associated with the prognosis and metastasis of patients with cervical squamous cell carcinoma (SCC) at the IB2 stage.
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.