Vascular endothelial growth factor C (VEGF-C) has been reported to be responsible for the lymphatic vessel density, tumor staging and lymph node metastasis, resulting in the failure of nasopharyngeal carcinoma (NPC) after radiotherapy.
The aim of this study was to investigate the expression of MMP-9 and VEGF-C at both mRNA and protein levels in breast cancer and to correlate with lymph node metastasis and other clinicopathological characteristics.
Downregulation of LSD1 expression inhibits metastatic potential of gastric cancer cells, and VEGF-C-mediated activation of PI3K/AKT signaling pathway, which may be an important mechanism for inhibiting lymph node metastasis in gastric cancer cells.
Furthermore, patients with high expressions of VEGF-C and Twist (V + T+) had significantly increased lymph node metastasis, higher clinical stage, and worse disease-free survival, DFS (P = 0.001) and overall survival, OS (P = 0.011).
The results revealed a significantly increased sVEGF-C level in patients with GBC compared with the healthy donors, however no statistically significant difference was identified between patients with GBC and chronic cholecystitis. sVEGF-C levels were associated with lymph node metastasis in GBC and presented a positive correlation with VEGF-C expression and lymphatic vessel density (LVD) in patients with GBC.
In particular, VEGF-C is specific to lymphatic vessel development, and VEGF-C expression levels have been found to directly correlate with lymph node metastasis in OSCC.
The results that Rg3 remarkably inhibited the expression of vascular endothelial growth factor-C (VEGF-C) protein in PTC cells and VEGF-A protein in anaplastic thyroid cancer (ATC) cells and decreased the staining of CD31 in PTC and ATC tumors hinted that Rg3 might inhibit the lymph node metastasis in PTC and angiogenesis in ATC.
Because vascular endothelial growth factor (VEGF)-C is known as a critical mediator of lymph node metastasis, we measured the expression level of VEGF-C mRNA in EOC tissues and thus identified a positive correlation between TBL1XR1 and VEGF-C mRNA levels.
The volume of lymph node metastases from B16-F10 experimental melanomas was reduced by 39% in orlistat-treated animals as well as the expression of VEGF-C in these tissues.
In vitro experiments demonstrated that TBL1XR1 can regulate the expression of vascular endothelial growth factor C and epithelial-mesenchymal transition proteins, thus mediate the process of lymph node metastasis.
The expression levels of MTA1 and VEGF-C in ESCC exhibited a positive correlation in ESCC, which may co-promote lymph angiogenesis and lymph node metastasis in ESCC; therefore, they may be used as biomarkers for determining the prognosis of ESCC.
In NSCLC tissues, the expression of HGF‑α, c‑Met or VEGF‑C was significantly correlated with the LMVD (P=0.045, 0.002 and 0.001, respectively), and lymph node metastasis was more common in HGF‑α, c‑Met or VEGF‑C‑positive groups (P=0.020, 0.020 and 0.009, respectively).
While combined high expression of PKM2 and VEGF-C was found to be associated with worse histological grade, more lymph node metastasis, more lymphovascular invasion, shorter progression free survival (PFS), and poorer overall survival (OS) in human breast cancer.
Immunohistochemical studies of breast cancer tumour tissue have reported a relation between the increased expression of vascular endothelial growth factor-C (VEGF-C) and the risk of lymph node metastasis.
It has been shown in many clinical studies that the level of vascular endothelial growth factor-C (VEGF-C) positively correlates with lymph node metastasis.
EMP1 expression decreased in breast cancer and correlated significantly with lymph node metastasis, clinic stage, histological grade, and poor overall survival, T stages, suggesting that EMP1 may play important roles as a negative regulator to breast cancer MCF-7 cell by regulating the expression of caspase 9 and VEGFC protein.