Research Papers:

SH003 represses tumor angiogenesis by blocking VEGF binding to VEGFR2

Hyeong Sim Choi, Min Kyoung Kim, Kangwook Lee, Kang Min Lee, Youn Kyung Choi, Yong Cheol Shin, Sung-Gook Cho _ and Seong-Gyu Ko

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Oncotarget. 2016; 7:32969-32979. https://doi.org/10.18632/oncotarget.8808

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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

Correspondence to:

Sung-Gook Cho, e-mail: [email protected]

Seong-Gyu Ko, e-mail: [email protected]

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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