The relationship between vimentin protein expression in endothelial cells and contrast-enhanced ultrasound characters in VETC (+ ) hepatocellular carcinoma
10.3760/cma.j.issn.0253-3766.2018.02.005
- VernacularTitle: VETC(＋)肝癌内皮细胞中波形蛋白的表达及其与超声造影表现的关系
- Author:
Chunyong LAN
1
;
Bing LING
1
;
Wenwen GUO
2
;
Wu YIN
2
;
Xiaogang ZHONG
3
;
Yamin HAN
3
;
Xiaofeng DONG
4
Author Information
1. Department of Ultrasound, the People′s Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, China
2. Department of Pathology, the People′s Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, China
3. Gastroenterological Surgery, the People′s Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, China
4. Hepatobiliary Surgery, the People′s Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, China
- Publication Type:Clinical Trail
- Keywords:
Carcinoma, hepatocellular;
Contrast-enhanced ultrasound;
VETC;
Angiopoietin-2;
Vimentin
- From:
Chinese Journal of Oncology
2018;40(2):105-109
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To detect the possible molecular mechanisms of the formation of vessels that encapsulated tumor clusters (VETC) and identify the relationship between vimentin protein expression in endothelial cells and contrast-enhanced ultrasound characters in VETC (+ ) hepatocellular carcinoma (HCC).
Methods:A total of 64 paraffin embedded HCC tissue samples were collected, all of which the tumor diameters were between 2 cm and 5 cm measured by the preoperative ultrasound. Immunohistochemistry staining for CD34 was used to detect the formation of VETC and the expressions of angiopoietin-2 (Ang-2) and vimentin were also determined. Human umbilical vein endothelial cells (HUVECs) were treated with 150 ng/ml recombinant human Ang-2 protein (rhAng-2) at various times and the protein expression of vimentin was detected by western blot assay. The contrast-enhanced ultrasound characters were also analyzed in both VETC (+ ) and VETC (-) HCC.
Results:Tumor clusters encapsulated by vessels to form cobweb-like networks, which were identified as VETC phenotype, were observed in 27 HCC tissues (42.18%). In VETC (+ ) HCC tissues, Ang-2 was overexpressed in tumor cells and endothelial cells while vimentin was only upregulated in endothelial cells. With the treatment of 150 ng/ml rhAng-2 protein, the expression of vimentin in HUVECs was 0.878±0.102 and 0.918±0.092 at 12 h and 36 h, significantly upregulated when compared to the 0.322±0.061 at 6 h (P<0.01). In contrast-enhanced ultrasound, a crack and tendon-like filling character was observed in VETC (+ ) HCC during the arterial-phase, while the large scale and diffuse-like filling character was observed in VETC (-) HCC. The filling time of unit diameter in VETC (+ ) HCC was (3.95±0.22)s, significantly longer than (2.28±0.27)s of VETC (-) HCC (P<0.01).
Conclusions:The overexpressions of Ang-2 and vimentin are positively correlated with the formation of VETC and considered as potential therapeutic targets of VETC (+ ) HCC. The crack and tendon-like filling characters in arterial-phase of contrast-enhanced ultrasound indicates the VETC (+ ) HCC.
