Next Article in Journal
Functional and Preliminary Characterisation of Hydrocolloid from Tamarillo (Solanum betaceum Cav.) Puree
Previous Article in Journal
Water Assisted Growth of C60 Rods and Tubes by Liquid–Liquid Interfacial Precipitation Method

Pristimerin, a Triterpenoid, Inhibits Tumor Angiogenesis by Targeting VEGFR2 Activation

Jiangsu Center for Drug Screening, China Pharmaceutical University, Nanjing 210009, Jiangsu, China
The Secondary Affiliated Hospital of Nanjing Medical University, Nanjing 210011, Jiangsu, China
Department of New Drug Screening, Jiangsu Chia-tai Tianqing Pharmaceutical Co., Ltd, Nanjing 210042, Jiangsu, China
Key Laboratory of Drug Quality Control and Pharmacovigilance, Ministry of Education, Nanjing 210009, Jiangsu, China
Authors to whom correspondence should be addressed.
Molecules 2012, 17(6), 6854-6868;
Received: 9 April 2012 / Revised: 11 May 2012 / Accepted: 15 May 2012 / Published: 5 June 2012
(This article belongs to the Section Natural Products Chemistry)
Pristimerin is a triterpenoid isolated from Celastrus and Maytenus spp. that has been shown to possess a variety of biological activities, including anti-cancer activity. However, little is known about pristimerin’s effects on tumor angiogenesis. In this study, we examined the function and the mechanism of this compound in tumor angiogenesis using multiple angiogenesis assays. We found that pristimerin significantly reduced both the volume and weight of solid tumors and decreased angiogenesis in a xenograft mouse tumor model in vivo. Pristimerin significantly inhibited the neovascularization of chicken chorioallantoic membrane (CAM) in vivo and abrogated vascular endothelial growth factor (VEGF)-induced microvessel sprouting in an ex vivo rat aortic ring assay. Furthermore, pristimerin inhibited the VEGF-induced proliferation, migration and capillary-like structure formation of human umbilical vascular endothelial cells (HUVECs) in a concentration-dependent manner. Mechanistic studies revealed that pristimerin suppressed the VEGF-induced phosphorylation of VEGF receptor 2 kinase (KDR/Flk-1) and the activity of AKT, ERK1/2, mTOR, and ribosomal protein S6 kinase. Taken together, our results provide evidence for the first time that pristimerin potently suppresses angiogenesis by targeting VEGFR2 activation. These results provide a novel mechanism of action for pristimerin which may be important in the treatment of cancer. View Full-Text
Keywords: pristimerin; angiogenesis; cancer; KDR/Flk-1; AKT/mTOR pristimerin; angiogenesis; cancer; KDR/Flk-1; AKT/mTOR
Show Figures

Figure 1

MDPI and ACS Style

Mu, X.; Shi, W.; Sun, L.; Li, H.; Jiang, Z.; Zhang, L. Pristimerin, a Triterpenoid, Inhibits Tumor Angiogenesis by Targeting VEGFR2 Activation. Molecules 2012, 17, 6854-6868.

AMA Style

Mu X, Shi W, Sun L, Li H, Jiang Z, Zhang L. Pristimerin, a Triterpenoid, Inhibits Tumor Angiogenesis by Targeting VEGFR2 Activation. Molecules. 2012; 17(6):6854-6868.

Chicago/Turabian Style

Mu, Xianmin, Wei Shi, Lixin Sun, Han Li, Zhenzhou Jiang, and Luyong Zhang. 2012. "Pristimerin, a Triterpenoid, Inhibits Tumor Angiogenesis by Targeting VEGFR2 Activation" Molecules 17, no. 6: 6854-6868.

Find Other Styles

Article Access Map by Country/Region

Only visits after 24 November 2015 are recorded.
Back to TopTop