Expert opinion VEGF plays an important role in sustaining the development and progression of lung cancer and it might represent an attractive target for therapeutic strategies.
HIF2A rs13419896 and VEGFArs833061 were significantly related to lung cancer risk, with possible interaction between polymorphisms and cigarette smoking.
We thus measured the levels of VEGF and endocan in the pleural effusion and serum samples of patients with lung cancer (n = 59) and those with tuberculosis (n = 32) by enzyme-linked immunosorbent assay.
Gain and loss-of-function studies were performed to investigate the effects of microRNA-130b, peroxisome proliferator-activated receptor γ (PPARγ) or vascular endothelial growth factor-A (VEGF-A) on biological functions of lung cancer cells using in vitro and in vivo approaches.
Collectively, our data suggested that VEGFA contributes to lung cancer progression by inducing a network of angiogenic factors, which might offer potential for therapeutic intervention.
Our results show that miRNAs-mediated FOXO3a/VEGF/CCL2 signaling plays a prominent role in LCCs-mediated NFs into CAFs, which may have clinical implications for providing novel biomarker(s) and potential therapeutic target(s) of lung cancer in the future.
To compare iodine content (IC) of solitary lung cancer using dynamic measurements of CT attenuation (Hounsfield Units, HU) and to correlate their quantitative CT data with expressions of vascular endothelial growth factor (VEGF), epidermal growth factor receptor (EGFR) and hypoxia-inducible factor-1α (HIF-1α) using immunostaining methods.
The VEGF pathway has become an important therapeutic target in lung cancer, where VEGF has long been established as a potent pro-angiogenic growth factor expressed by many types of tumors.
Based on the reliable and reproducible animal model, our findings indicate that knock-down of Livin inhibits cell growth and invasion through blockade of the VEGF and MMPs pathways in lung cancer cells in vitro, and inhibits tumorigenesis and metastasis of lung cancer in vivo, suggesting that Livin is a promising antitumor target.
Many studies have shown that vascular endothelial growth factor (VEGF), especially the human VEGF-A165 (hVEGF-A165) isoform, is a key proangiogenic factor that is overexpressed in lung cancer.
The aberrant signaling activation of vascular endothelial growth factor receptor (VEGFR) and urokinase plasminogen activator (uPA) is a common characteristic of many tumors, including lung cancer.
For the diagnosis of malignant pleural effusion caused by lung cancer, LUNX mRNA exhibited higher sensitivity (80%), when compared with vascular endothelial growth factor mRNA (65%), carcinoembryonic antigen (67%) and Cyfra21-1 (61%), with the same specificity (95%).
Unlike the situation with the -2578C/A polymorphism, the VEGF-460C/T polymorphism is not associated with the risk of lung cancer in neither Asians nor Caucasians.
We investigated whether VEGF +936C>T polymorphism influences lung cancer risk and lung cancer patients' overall survival (OS) using pooled odds ratios (ORs) and hazard ratios (HRs) with their corresponding 95% confidence intervals (CI) under different genetic models.
Suppression of lung cancer cell invasion by LKB1 is due to the downregulation of tissue factor and vascular endothelial growth factor, partly dependent on SP1.
More studies are needed to detect VEGF-634G/C and VEGF -2578 polymorphisms and their association with lung cancer in different ethnic populations incorporated with environmental exposures.
rs833061 and rs699947 on promoter gene of vascular endothelial growth factor (VEGF) and associated lung cancer susceptibility and survival: a meta-analysis.
More studies are needed to detect VEGF-460C/T polymorphism and its association with lung cancer in different ethnic populations incorporated with environmental exposures.