Tumor-secreted vascular endothelial growth factor A increases the pulmonary metastasis from nasopharyngeal carcinoma
10.3760/cma.j.issn.1673-0860.2018.01.006
- VernacularTitle: 肿瘤源性血管内皮生长因子A促进鼻咽癌肺转移的实验研究
- Author:
Yi FANG
1
;
Chang XU
2
;
Dawei LI
1
;
Ziling WANG
1
;
Lu ZHANG
3
;
Peng WU
2
;
Zhenzhen WANG
4
;
Han DU
2
;
Wenfeng LI
5
;
Zhisu LIAO
2
Author Information
1. First Clinical Institute, Wenzhou Medical University, Wenzhou 325000, China
2. Department of Otorhinolaryngology, First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China
3. Department of Otorhinolaryngology, Second People′s Hospital of Ningbo City, Ningbo 315010, China
4. Department of Otorhinolaryngology, Ningbo City Medical treatment Center Lihuili Hospital, Ningbo 315000, China
5. Department of Radiotherapy and Chemotherapy, First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China
- Publication Type:Journal Article
- Keywords:
Vascular endothelial growth factor A;
Nasopharyngeal neoplasms;
Lung neoplasmas;
Neoplasmas metastasis
- From:
Chinese Journal of Otorhinolaryngology Head and Neck Surgery
2018;53(1):27-33
- CountryChina
- Language:Chinese
-
Abstract:
Objective:Vascular endothelial growth factor A (VEGFA) was investigated as the key protein which might promote the specific metastasis progress of nasopharyngeal carcinoma.
Methods:Sixteen specimens of pulmonary metastasis carcinoma and counterparts in primary nasopharyngeal carcinoma tissue were collected from patients. The expression of VEGFA through immunohistochemistry was investigated.VEGFA was knocked down by siRNA in two cell lines of nasopharyngeal carcinoma (CNE-1 and 5-8F), MTT and Transwell test were used to explore the role of VEGFA in praxiology. Then shRNA was used to cultivate the stable CNE-1 cell line with down-regulated-expression of VEGFA. The nude mice models were built through tail vein injection of specific nasopharyngeal carcinoma cells, and lungs were collected to perform further metastasis analysis.
Results:Previous genetic studies showed that VEGFA had higher expression in metastasis tissue, and the result was validated in the present study using immunohistochemistry. The percentage of positive cells was 84.8% in pulmonary metastasis group, 51.5% in primary tissue group (t=8.639, P<0.05), average optical density was 0.154 in pulmonary metastasis group, 0.061 in primary tissue group (t=18.791, P<0.05). Low expression of VEGFA inhibited cell viability of optical density value of CNE-1 in siRNA gourp was 0.715, 0.902 in control group (t=7.274, P<0.05); 5-8F in siRNA group was 0.715, 0.935 in control group (t=7.751, P<0.05). Number counting suppressed migration of CNE-1 in siRNA group was 52 per high-power lens, 124 per high-power lens in control group (t=29.380, P<0.05), 5-8F in siRNA group was 65 per high-power lens, 155 per high-power lens in control group (t=18.181, P<0.05). Number counting invasion of CNE-1 in siRNA gourp was 38 per high-power lens, 86 per high-power lens in control group (t=27.665, P<0.05), 5-8F in siRNA group was 52 per high-power lens, 116 per high-power lens in control group (t=40.972, P<0.05) in vitro. Furthermore, knock-down of VEGFA in nasopharyngeal carcinoma reduced the pulmonary metastasis in vivo. Number counting of tumor volumes in shRNA group was 2.4, and 11.0 in control group (t=6.143, P<0.05); average optical density of immunohistochemistry in shRNA group was 0.033, and 0.176 in control group (t=15.734, P<0.05).
Conclusions:Results above reveal the overexpression of VEGFA in nasopharyngeal carcinoma can facilitate the pulmonary metastasis. Targeting VEGFA may provide a new biomarker of clinical study.
