CXCR7 is up-regulated in human and murine hepatocellular carcinoma and is specifically expressed by endothelial cells

2012 ◽  
Vol 48 (1) ◽  
pp. 138-148 ◽  
Author(s):  
Justin Monnier ◽  
Mathieu Boissan ◽  
Annie L’Helgoualc’h ◽  
Marie-Lise Lacombe ◽  
Bruno Turlin ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Endothelial Cells

miR-3156-5p Enhances Hypoxia-Induced Angiogenesis in Hepatocellular Carcinoma via Modulating the SOCS5/HIF-1α/VEGF Pathway

2021 ◽  
Author(s):  
Bin Tie ◽  
Zheng Guo ◽  
Li Li ◽  
Wenhui Wang ◽  
Rong Liu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Endothelial Cells ◽  
Colony Formation ◽  
Cell Counting ◽  
Angiogenic Potential ◽  
Reverse Transcription Pcr ◽  
Vegf Pathway ◽  
Formation Experiment ◽  
Hcc Cells

Abstract Background: MicroRNAs (miRNAs) are dysregulated in hypoxia-induced hepatocellular carcinoma (HCC). This study probed the regulatory mechanism of miR-3156-5p on HCC under hypoxia. Methods: HCC cells (HepG2) were exposed to normoxia or hypoxia, and the conditioned medium (CM) of HepG2 was applied. Quantitative reverse transcription PCR (qRT-PCR) was implemented to analyze the miR-3156-5p profile. The cell counting kit-8 (CCK-8) assay and the colony formation experiment were conducted to measure cell proliferation, colony formation, and angiogenesis. Results: The results manifested that miR-3156-5p was up-regulated in HCC cells and endothelial cells under hypoxia, and up-regulating miR-3156-5p boosted HCC cell proliferation, endothelial cell angiogenesis, and HIF-1α/VEGF expression. Conclusions: miR-3156-5p activates the HIF-1α/VEGF pathway by hampering SOCS5, thereby enhancing the angiogenic potential of hypoxia-induced endothelial cells in HCC cells.

scholarly journals Apatinib targets both tumor and endothelial cells in hepatocellular carcinoma

2018 ◽  
Vol 7 (9) ◽  
pp. 4570-4583 ◽  
Author(s):  
Chaoxu Yang ◽  
Shukui Qin
Keyword(s):  
Hepatocellular Carcinoma ◽  
Endothelial Cells

scholarly journals Overexpression of SULT2B1b Promotes Angiogenesis in Human Gastric Cancer

2016 ◽  
Vol 38 (3) ◽  
pp. 1040-1054 ◽  
Author(s):  
Wen Chen ◽  
Haiyu Zhou ◽  
Lei Ye ◽  
Baogen Zhan
Keyword(s):  
Gastric Cancer ◽  
Hepatocellular Carcinoma ◽  
Endothelial Cells ◽  
Cancer Progression ◽  
Human Gastric Cancer ◽  
Qrt Pcr ◽  
Diagnosis And Prognosis ◽  
Promising Strategy ◽  
Oncogenic Protein ◽  
Gastric Cancer Progression

Background/Aims: Overexpression of cytosolic sulfotransferase 2B1b (SULT2B1b) has been commonly found in colorectal and hepatocellular carcinoma, suggesting that SULT2B1b might act as a potential oncogenic protein. However, its clinical significance and biological role in gastric cancer progression remain largely unknown. Methods: Expressions of SULT2B1b in clinical gastric cancer (GC) samples were examined using qRT-PCR and Western blot. Results: SULT2B1b was markedly overexpressed in human GC samples, and positively correlated with vessel density and associated with poor clinical features. We also demonstrated that overexpression of SULT2B1b resulted in increased tumor angiogenesis and tumor growth in mouse GC models. In addition, ablation of SULT2B1b in human GC cells lines BGC823 and MKN45 decreased the capability of the cells to recruit endothelial cells. Moreover, depletion of SULT2B1b in GC cells reduced VEGF-A expression by downregulating SP1 and AP2. Conclusion: Our results suggested that the SULT2B1b-mediated angiogenic pathway could serve as biomarkers for GC diagnosis and prognosis, and suppressing SULT2B1b-mediated angiogenic signaling might be a promising strategy for developing novel GC treatment.

scholarly journals Vector-mediated Tum-5 expression in neovascular endothelial cells for treating hepatocellular carcinoma

2017 ◽  
Vol 13 (4) ◽  
pp. 1521-1525
Author(s):  
Chun Li ◽  
Xingang Guan ◽  
Boqian Sun ◽  
Mingyao Ma ◽  
Peng Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Endothelial Cells
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