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Open Access Research article

Particled Mica, STB-HO has chemopreventive potential via G1 arrest, and inhibition of proliferation and vascular endothelial growth factor receptor 2 in HCT colorectal cancer cells

Sung-Yun Cho1, Hyo-Jeong Lee1, Sun-Mi Cho1, Bonglee Kim1, Yeon Kwon Jung2 and Sung-Hoon Kim1*

Author Affiliations

1 Cancer Preventive Material Development Research Center, College of Korean Medicine, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, 130-701, Seoul, South Korea

2 SeoBong Biobestech Co, 831 Yeoksam-dong, Gangnam-gu, Ltd.Hye Cheon Bldg #401, 135-080, Seoul, Republic of Korea

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BMC Complementary and Alternative Medicine 2013, 13:189  doi:10.1186/1472-6882-13-189

Published: 24 July 2013



Though Mica, a thin and sheet like mineral, has been used as a mineral medicine for treatment of bleeding, dysentery and inflammation in traditional medicine including Ayurveda, the biological evidences of Mica were not clearly elucidated so far. Thus, in the present study, the antitumor mechanism of particled Mica (STB-HO) was examined in colorectal cancers.


Athymic nude mice were inoculated with HCT116 colon cancer cells and orally administered STB-HO daily for 41 days, and HCT116 and human umbilical vein endothelial cells (HUVECs) were treated with STB-HO for 0 ~ 24 hours to perform immunoblotting, cytotoxicity assay, FACs analysis and measurement of matrix metalloproteinase 9 (MMP-9) secretion and other experiments. Significant differences of all date were evaluated using Student’s t-test and a Turkey-Kramer multiple-comparison post test.


STB-HO significantly suppressed the tumor volume and weight in athymic nude mice inoculated with HCT116 cells at a dose of 100 mg/kg. Thus, the in vivo antitumor mechanism of STB-HO was to elucidated in vitro as well. STB-HO exerted cytotoxicity in HCT116, SW620 and HCT15 colorectal cancer cells. Also, STB-HO increased G1 cell population in a time and concentration dependent manner, enhanced the expression of p21, p27, p53 as cyclin dependent kinase (CDK) inhibitors, attenuated the expression of proliferating cell nuclear antigen (PCNA) and cyclin D1 and also reduced the production of vascular endothelial growth factor (VEGF) and matrix metalloproteinase 9 (MMP-9) in HCT116 cells. Consistently, STB-HO suppressed the phosphorylation of VEGFR2 in HCT116, SW620 and HCT15 cells. Also, STB-HO inhibited the VEGF mediated proliferation and also attenuated the phosphorylation of VEGFR2 and Akt in human umbilical vein endothelial cells (HUVECs).


Collectively, these findings suggest that STB-HO has chemopreventive potential via G1 arrest and inhibition of proliferation and VEGFR2 in HCT116 colorectal cancer cells.

Mica; VEGFR; Colon cancer; G1 arrest; Cell proliferation