Upon interactions between experimental and predicted candidate targets, we identified three key candidate targets of RO against NPC: VEGFA, TP53, and HSPA8, by calculating the nodes' topological features.
For patients with advanced NPC who refuse standard radiotherapy and chemotherapy, apatinib monotherapy may be a suitable treatment option to improve symptoms and quality of life even in those with vascular endothelial growth factor receptor-negative tumors.
<b>Methods:</b> We conducted a systematic literature search of PubMed, Embase, and the Cochrane Library for observational studies published until June, 2018 to identify observational studies on the prognostic effect of tissue VEGF expression or serum VEGF level on the survival of NPC.
Blockage of store-operated Ca<sup>2+</sup> entry antagonizes Epstein-Barr virus-promoted angiogenesis by inhibiting Ca<sup>2+</sup> signaling-regulated VEGF production in nasopharyngeal carcinoma.
Additionally, knockdown of FOXCUT significantly inhibited proliferation and migration of nasopharyngeal carcinoma cell lines and resulted in downregulated expression of the matrix metalloproteinase 7 and matrix metalloproteinase 9, as well as vascular endothelial growth factor A and β-catenin.
In this study, we confirmed sunitinib induced downregulation of its targets, such as vascular endothelial growth factor, platelet-derived growth factor, and c-kit in multiple-drug-resistant nasopharyngeal carcinoma cell line CNE2/DDP and hepatoma cell line HepG2.
In conclusion, the VEGF-460T/C gene polymorphism may negatively affect the clinical outcomes of patients with NPC and may be considered a potential prognostic factor for this disease.
Compared with vector-alone control cells, BLU stable transfectants, derived from poorly-differentiated NPC HONE1 cells, suppress VEGF165, VEGF189 and TSP1 expression at both the RNA and protein levels, and significantly reduce the secreted VEGF protein in these cells, reflecting an unknown regulatory mechanism mediated by the BLU gene in NPC.
Treatment of nasopharyngeal carcinoma cells with TFAP2A siRNA dramatically inhibited the expression and the release of VEGF protein but did not change the level of PEDF protein, resulting in a significant reduction of the ratio of VEGF/PEDF.
In addition, protein concentration of VEGF in NPC biopsies with -1486 CC genotype was significantly increased compared patients with -1486 TT genotype.
These results therefore indicate that nicotine promotes proliferation of human NPC cells in vitro through simultaneous modulation of α7AChR, HIF-1α, ERK and VEGF/PEDF signaling and suggest that the related molecules such as HIF-1α might be the potential therapeutic targets for tobacco-associated diseases such as nasopharyngeal carcinomas.
Zoledronic acid inhibits proliferation and impairs migration and invasion through downregulating VEGF and MMPs expression in human nasopharyngeal carcinoma cells.
The levels of interleukin (IL)-6, IL-8, interferon-inducible protein 10 (IP-10), tumor necrosis factor (TNF)-α, vascular endothelial growth factor (VEGF), and macrophage inflammatory protein (MIP)-3α were significantly elevated in patients with NPC; but the stem cell factor (SCF) levels were significantly lower.
However, PEDF decreased vascular endothelial growth factor (VEGF) in NPC cell lines by downregulation of hypoxia-inducible factor 1a, a crucial transcriptional factor for VEGF expression, as demonstrated by western blotting and immunofluorescent staining assay.
Our findings suggest that the expression of CXCR4 and VEGF is associated with metastatic progression, and that VEGF expression is a valuable prognostic marker in nasopharyngeal carcinoma.
Multivariate analysis indicated that both survivin and VEGF over-expression in NPC tumor tissues were strong independent factors of poor prognosis in NPC patients.