scholarly journals Plumbagin restrains hepatocellular carcinoma angiogenesis by suppressing the migration and invasion of tumor-derived vascular endothelial cells

Oncotarget ◽  
2017 ◽  
Vol 8 (9) ◽  
pp. 15230-15241 ◽  
Author(s):  
YanFei Wei ◽  
Qi Yang ◽  
Yuan Zhang ◽  
TieJian Zhao ◽  
XueMei Liu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Migration And Invasion ◽  
Vascular Endothelial

Enhanced CD34 expression of sinusaid-like vascular endothelial cells in hepatocellular carcinoma

1996 ◽  
Vol 46 (10) ◽  
pp. 751-756 ◽  
Author(s):  
Shunjin Cui ◽  
Hiroshi Hano ◽  
Akihiko Sakata ◽  
Toru Harada ◽  
Tiecheng Liu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Cd34 Expression

scholarly journals Hepatitis B Virus preS2 Domain Promotes Angiogenesis in Hepatocellular Carcinoma via Transcriptional Activation of VEGFA Promoter

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Fang Luan ◽  
Bin Liu ◽  
Xiangrui Guo ◽  
Wang Yong
Keyword(s):  
Hepatocellular Carcinoma ◽  
Endothelial Cells ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Vascular Endothelial Cells ◽  
Luciferase Assay ◽  
Luciferase Reporter ◽  
Endothelial Cell Proliferation ◽  
Vascular Endothelial ◽  
B Virus

: Angiogenesis is closely related to the development and progression of hepatocellular carcinoma (HCC). Angiogenic factors have been confirmed to be overexpressed in HCC. The hepatitis B virus preS2 domain is a transactivator that plays an important role in hepatitis B virus (HBV)-related HCC. Here, we aimed to investigate the potential of the preS2 domain in inducing angiogenesis in HCC. A total of 25 cases of pathologically confirmed HCC were screened. The levels of preS2, CD34, and vascular endothelial growth factor A (VEGFA) in HCC samples were evaluated by immunohistochemistry (IHC). The proliferation of vascular endothelial cells was detected by CCK-8. Besides, VEGFA was analyzed by Western blot in HCC cells. The effect of preS2 on the VEGFA promoter was measured by dual-luciferase reporter assays. We found that preS2 domain-positive HCCs had significantly higher microvessel density (MVD) and VEGFA expression than preS2 domain-negative HCCs. Overexpression of preS2 upregulated VEGFA expression in HepG2 and activated vascular endothelial cell proliferation. However, blocking preS2 expression reduced VEGFA expression in HepG2.2.15 and inhibited the proliferation of vascular endothelial cells. In addition, a dual-luciferase assay indicated that the preS2 domain could activate VEGFA promoter activity. In conclusion, we showed that the expression of the preS2 domain promotes angiogenesis by transactivating the VEGFA promoter in HCC.

Knockdown of HIF-1α and IL-8 induced apoptosis of hepatocellular carcinoma triggers apoptosis of vascular endothelial cells

APOPTOSIS ◽  
2015 ◽  
Vol 21 (1) ◽  
pp. 85-95 ◽  
Author(s):  
Sung Hoon Choi ◽  
Jun Yong Park ◽  
Wonseok Kang ◽  
Seung Up Kim ◽  
Do Young Kim ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Induced Apoptosis

siVEGF-loaded nanoparticle uptake by tumor-associated vascular endothelial cells for hepatocellular carcinoma

Nanomedicine ◽  
2020 ◽  
Vol 15 (13) ◽  
pp. 1297-1314
Author(s):  
Bohui Xu ◽  
Yan Zhang ◽  
Han Yang ◽  
Tingting Liu ◽  
Youjia Lu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Carcinoma Cells ◽  
Vascular Endothelial ◽  
Vegf Mrna ◽  
Antiangiogenic Effect ◽  
Tumor Bearing ◽  
Ea.Hy926 Cells

Aim: This study examined nanoparticle entry into tumor-associated vascular endothelial cells during transport to hepatocellular carcinoma cells and tumors. Materials & methods: siVEGF was loaded into CS-SS-9R/BSA-cRGD nanoparticles (CBc NPs). The intracellular uptake, gene silencing efficiency, antiproliferation and antiangiogenic effect of the NPs were performed on EA.hy926 cells. In vivo antitumor and antiangiogenic effects were investigated in Bel-7402 tumor-bearing nude mice. Results: siVEGF-loaded CBc NPs entered EA.hy926 cells and suppressed their proliferation and capillary formation. The NPs also inhibited tumor proliferation and angiogenesis in tumor-bearing mice, which attributed to the downregulation of VEGF mRNA expression in tumor tissue. Conclusion: The uptake of siVEGF-loaded CBc NPs by tumor-associated vascular endothelial cells made important contributions in controlling the progression of hepatocellular carcinoma.

scholarly journals Cell death in a co-culture of hepatocellular carcinoma cells and human umbilical vascular endothelial cells in a medium lacking glucose and arginine

2016 ◽  
Vol 13 (1) ◽  
pp. 258-262 ◽  
Author(s):  
Minoru Tomizawa ◽  
Fuminobu Shinozaki ◽  
Yasufumi Motoyoshi ◽  
Takao Sugiyama ◽  
Shigenori Yamamoto ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Endothelial Cells ◽  
Cell Death ◽  
Vascular Endothelial Cells ◽  
Carcinoma Cells ◽  
Vascular Endothelial ◽  
Hepatocellular Carcinoma Cells

The Endothelial Cell and the Factor VIII Bypassing Activity of Prothrombin Complex Concentrate

1988 ◽  
Vol 60 (02) ◽  
pp. 226-229 ◽  
Author(s):  
Jerome M Teitel ◽  
Hong-Yu Ni ◽  
John J Freedman ◽  
M Bernadette Garvey
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Factor Viii ◽  
Prothrombin Complex Concentrate ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Monolayer Cultures ◽  
Coagulant Activity ◽  
Time Courses ◽  
Privileged Site

SummarySome classical hemophiliacs have a paradoxical hemostatic response to prothrombin complex concentrate (PCC). We hypothesized that vascular endothelial cells (EC) may contribute to this “factor VIII bypassing activity”. When PCC were incubated with suspensions or monolayer cultures of EC, they acquired the ability to partially bypass the defect of factor VIII deficient plasma. This factor VIII bypassing activity distributed with EC and not with the supernatant PCC, and was not a general property of intravascular cells. The effect of PCC was even more dramatic on fixed EC monolayers, which became procoagulant after incubation with PCC. The time courses of association and dissociation of the PCC-derived factor VIII bypassing activity of fixed and viable EC monolayers were both rapid. We conclude that EC may provide a privileged site for sequestration of constituents of PCC which express coagulant activity and which bypass the abnormality of factor VIII deficient plasma.

Alterations in Vascular Endothelial Cell-related Plasma Proteins In Thalassaemic Patients and their Correlation with Clinical Symptoms

1995 ◽  
Vol 74 (04) ◽  
pp. 1045-1049 ◽  
Author(s):  
P Butthep ◽  
A Bunyaratvej ◽  
Y Funahara ◽  
H Kitaguchi ◽  
S Fucharoen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Immunosorbent Assay ◽  
Plasma Proteins ◽  
Clinical Symptoms ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Enzyme Linked Immunosorbent Assay ◽  
Vascular Endothelial ◽  
Leg Ulcers

SummaryAn increased level of plasma thrombomodulin (TM) in α- and β- thalassaemia was demonstrated using an enzyme-linked immunosorbent assay (ELISA). Nonsplenectomized patients with β-thalassaemia/ haemoglobin E (BE) had higher levels of TM than splenectomized cases (BE-S). Patients with leg ulcers (BE-LU) were found to have the highest increase in TM level. Appearance of larger platelets in all types of thalassaemic blood was observed indicating an increase in the number of younger platelets. These data indicate that injury of vascular endothelial cells is present in thalassaemic patients.

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