Home | About PM | Editorial board | Search | Ahead of print | Current Issue | Archives | Instructions | Subscribe | Advertise | Contact us |  Login 
Pharmacognosy Magazine
Search Article 
  
Advanced search 
 
ORIGINAL ARTICLE
Year : 2020  |  Volume : 16  |  Issue : 67  |  Page : 169-176

Cordyceps militaris fraction inhibits angiogenesis of hepatocellular carcinoma in vitro and in vivo


1 Department of Pharmacology, College of Pharmacy, Jinan University, Guangzhou, China
2 Biotechnological Institute of Chinese Materia Medica, Jinan University, Guangzhou, China
3 Department of Natural Product Chemistry, College of Pharmacy, Jinan University, Guangzhou, China
4 Biotechnological Institute of Chinese Materia Medica; Department of Natural Product Chemistry, College of Pharmacy, Jinan University, Guangzhou, China

Correspondence Address:
Liyan Song
Department of Pharmacology, College of Pharmacy, Jinan University, Guangzhou, 510632
China
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/pm.pm_347_19

Rights and Permissions

Background: Cordyceps militaris fraction (CMF) was found to inhibit the proliferation of chronic myeloid leukemia K562 cells, oral squamous carcinoma KB cells, and the metastasis of lung cancer cells. This study focuses on the activity of CMF against angiogenesis of hepatocellular carcinoma (HCC). Objectives: The objective of the study is to research the antiangiogenic activity of CMF in HCC cells and the underlying mechanism in vitro and in vivo. Materials and Methods: Transwell migration and invasion assays were used to measure the effects of CMF on migration and invasion of SMMC-7721 cells and human umbilical vein endothelial cells (HUVECs). Tube formation and rat aortic ring assays were used to assess the antiangiogenic potential of CMF. The antiangiogenic mechanism was detected by immunofluorescence and western blot analysis. The nude mice xenografted with SMMC-7721 cells were used to study the antiangiogenic activity of CMF and its underlying mechanism in vivo. Immunohistochemistry analysis was used to evaluate the effect of CMF on the expression of CD31, and western blot analysis was also performed to detect the expression of vascular endothelial growth factor (VEGF) and other related proteins in tumor tissues. Results: CMF inhibited the migration and invasion of SMMC-7721 cells and HUVECs and suppressed VEGF-induced tube formation of HUVECs and the formation of aortic ring capillaries of rats in a concentration-dependent manner. CMF attenuated the phosphorylation of VEGF receptor 2 (VEGFR2), Akt, and ERK in SMMC-7721 cells and HUVECs. CMF significantly inhibited tumor growth in nude mice xenografted with SMMC-7721 cells. CMF reduced the expression level of CD31, western blot analysis indicated that CMF downregulated the expression of VEGFR2 and attenuated the phosphorylation of Akt and ERK in the tumor tissues, which was consistent with the results obtained from in vitro study. Conclusion: CMF can inhibit the angiogenesis of HCC and the mechanism is associated with suppression of the VEGF/VEGFR2 signaling pathway.


[FULL TEXT] [PDF]*
Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed158    
    Printed2    
    Emailed0    
    PDF Downloaded29    
    Comments [Add]    

Recommend this journal