scholarly journals Dihydrodiosgenin inhibits endothelial cell-derived factor VIII and platelet-mediated hepatocellular carcinoma metastasis

2019 ◽  
Vol Volume 11 ◽  
pp. 4871-4882 ◽  
Author(s):  
Manjiao Zhuang ◽  
Guang Xin ◽  
Zeliang Wei ◽  
Shiyi Li ◽  
Zhihua Xing ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Endothelial Cell ◽  
Factor Viii ◽  
Carcinoma Metastasis

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.

LINC01348 suppresses hepatocellular carcinoma metastasis through inhibition of SF3B3-mediated EZH2 pre-mRNA splicing

Oncogene ◽  
2021 ◽  
Author(s):  
Yang-Hsiang Lin ◽  
Meng-Han Wu ◽  
Yi-Chung Liu ◽  
Ping-Chiang Lyu ◽  
Chau-Ting Yeh ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Mrna Splicing ◽  
Carcinoma Metastasis

Tumor cells derived-extracellular vesicles transfer miR-3129 to promote hepatocellular carcinoma metastasis by targeting TXNIP

2021 ◽  
Vol 53 (4) ◽  
pp. 474-485
Author(s):  
Yang Yang ◽  
Feifei Mao ◽  
Lei Guo ◽  
Jie Shi ◽  
Mengchao Wu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Cells ◽  
Extracellular Vesicles ◽  
Carcinoma Metastasis

Research on Mechanism of miRNA-22 Related with Hepatocellular Carcinoma Metastasis for Regulating Process of Tumor Protein P53

2021 ◽  
Vol 11 (11) ◽  
pp. 2115-2119
Author(s):  
Gang Pan ◽  
Min Xiao
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Invasion ◽  
Cell Activity ◽  
Rt Pcr ◽  
Transwell Assay ◽  
Hep2 Cell ◽  
Tumor Protein P53 ◽  
Carcinoma Metastasis ◽  
Invasion Capacity ◽  
P53 Mrna

The action of miRNA-22 related with HCC metastasis was analyzed in our study and the mechanism of miRNA-22 related with HCC metastasis was discussed. The HCC hep2 cell was transfected with miRNA-22 mimics and miRNA-22 NC instantaneously followed by analysis of cell migration by Transwell assay, cell viability by MTT and clone formation and cell apoptosis by flow cytometry. The action of miRNA-22 mimics and miRNA-22 on the expression of P53 mRNA in HCC Hep2 cell was detected by RT-PCR. The cell activity in miRNA-22 mimics group was significantly elevated compared with miRNA-22 NC group (P < 0.01). Meanwhile, the apoptotic rate, migrated and invaded capacity of HCC cell was significantly elevated (P < 0.01). The expression level of P53 mRNA was reduced (P < 0.01). In conclusion, overexpression of miRNA-22 could restrain the apoptosis of HCC hep2 cell and down-regulated the expression of P53 so as to prompt cell invasion capacity.

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