SH003 represses tumor angiogenesis by blocking VEGF binding to VEGFR2
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Hyeong Sim Choi1, Min Kyoung Kim1, Kangwook Lee1, Kang Min Lee1, Youn Kyung Choi2, Yong Cheol Shin3, Sung-Gook Cho4, Seong-Gyu Ko3
1Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul, Korea
2Jeju International Marine Science Center for Research and Education, Korea Institute of Ocean Science & Technology (KIOST), Jeju, Korea
3Department of Preventive Medicine, College of Korean Medicine, Kyung Hee University, Seoul, Korea
4Department of Biotechnology, Korea National University of Transportation, Jeungpyeong, Chungbuk, Korea
Sung-Gook Cho, e-mail: email@example.com
Seong-Gyu Ko, e-mail: firstname.lastname@example.org
Keywords: SH003, tumor angiogenesis, VEGF, VEGFR2, TCM
Received: December 18, 2015 Accepted: March 31, 2016 Published: April 18, 2016
Tumor angiogenesis is a key feature of cancer progression, because a tumor requires abundant oxygen and nutrition to grow. Here, we demonstrate that SH003, a mixed herbal extract containing Astragalus membranaceus (Am), Angelica gigas (Ag) and Trichosanthes Kirilowii Maximowicz (Tk), represses VEGF-induced tumor angiogenesis both in vitro and in vivo. SH003 inhibited VEGF-induced migration, invasion and tube formation in human umbilical vein endothelial cells (HUVEC) with no effect on the proliferation. SH003 reduced CD31-positive vessel numbers in tumor tissues and retarded tumor growth in our xenograft mouse tumor model, while SH003 did not affect pancreatic tumor cell viability. Consistently, SH003 inhibited VEGF-stimulated vascular permeability in ears and back skins. Moreover, SH003 inhibited VEGF-induced VEGFR2-dependent signaling by blocking VEGF binding to VEGFR2. Therefore, our data conclude that SH003 represses tumor angiogenesis by inhibiting VEGF-induced VEGFR2 activation, and suggest that SH003 may be useful for treating cancer.
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