Anticoagulant and FGF/FGFR signal activating activities of the heparinoid propylene glycol alginate sodium sulfate and its oligosaccharides

2016 ◽  
Vol 136 ◽  
pp. 641-648 ◽  
Author(s):  
Jian Wu ◽  
Meng Zhang ◽  
Yiran Zhang ◽  
Yangyang Zeng ◽  
Lijuan Zhang ◽  
...  
2014 ◽  
Vol 104 ◽  
pp. 23-28 ◽  
Author(s):  
Jian Wu ◽  
Xia Zhao ◽  
Li Ren ◽  
Yiting Xue ◽  
Chunxia Li ◽  
...  

2016 ◽  
Vol 144 ◽  
pp. 330-337 ◽  
Author(s):  
Yi-Ting Xue ◽  
Li Ren ◽  
Shuang Li ◽  
Lin-lin Wang ◽  
Xiao-Xi He ◽  
...  

Marine Drugs ◽  
2019 ◽  
Vol 17 (5) ◽  
pp. 257 ◽  
Author(s):  
He Ma ◽  
Peiju Qiu ◽  
Huixin Xu ◽  
Ximing Xu ◽  
Meng Xin ◽  
...  

Melanoma is one of the most malignant and aggressive types of cancer worldwide. Fibroblast growth factor 2 (FGF2) is one of the critical regulators of melanoma angiogenesis and metastasis; thus, it might be an effective anti-cancer strategy to explore FGF2-targeting drug candidates from existing drugs. In this study, we evaluate the effect of the marine drug propylene glycol alginate sodium sulfate (PSS) on FGF2-mediated angiogenesis and invasion. The data shows that FGF2 selectively bound to PSS with high affinity. PSS inhibited FGF2-mediated angiogenesis in a rat aortic ring model and suppressed FGF2-mediated invasion, but not the migration of murine melanoma B16-F10 cells. The further mechanism study indicates that PSS decreased the expression of activated matrix metalloproteinase 2 (MMP-2) and matrix metalloproteinase 9 (MMP-9), and also suppressed their activity. In addition, PSS was found to decrease the level of Vimentin in B16-F10 cells, which is known to participate in the epithelial–mesenchymal transition. Notably, PSS did not elicit any changes in cancer cell viability. Based on the results above, we conclude that PSS might be a potential drug to regulate the tumor microenvironment in order to facilitate the recovery of melanoma patients.


2014 ◽  
Vol 13 (4) ◽  
pp. 683-690 ◽  
Author(s):  
Pengli Li ◽  
Chunxia Li ◽  
Yiting Xue ◽  
Yang Zhang ◽  
Hongbing Liu ◽  
...  

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