Effect of methanol extracts of Cnidium officinale Makino and Capsella bursa-pastoris on the apoptosis of HSC-2 human oral cancer cells

Lee,Kyung-Eun; Shin,Ji-Ae; Hong,In-Sun; Cho,Nam-Pyo; Cho,Sung-Dae

doi:10.3892/etm.2012.871

Effect of methanol extracts of Cnidium officinale Makino and Capsella bursa-pastoris on the apoptosis of HSC-2 human oral cancer cells

Authors:
- Kyung-Eun Lee
- Ji-Ae Shin
- In-Sun Hong
- Nam-Pyo Cho
- Sung-Dae Cho
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Affiliations: Department of Oral Medicine, Chonbuk National University, Jeonju 561-756, Republic of Korea, Department of Oral Pathology, School of Dentistry, Institute of Oral Bioscience, BK21 Project, Chonbuk National University, Jeonju 561-756, Republic of Korea, Department of Veterinary Public Health, Laboratory of Stem Cell and Tumor Biology, Seoul National University, Seoul 151-742, Republic of Korea
Published online on: December 21, 2012 https://doi.org/10.3892/etm.2012.871
Pages: 789-792

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Abstract

Cnidium officinale Makino and Capsella bursa‑pastoris are used as traditional herbs with diverse medicinal effects, including the inhibition of inflammation, reduction of blood pressure and as diuretics, however, the anticancer effects of C. officinale Makino and C. bursa-pastoris are poorly defined. The aims of this study were to evaluate the effects of methanol extracts of C. officinale Makino (MECO) and methanol extracts of C. bursa‑pastoris (MECB) on the cell growth and apoptosis of HSC-2 human oral cancer cells. MECO and MECB caused growth inhibition and the induction of apoptosis in a concentration-dependent manner in HSC-2 cells. A marked reduction in specificity protein 1 (Sp1) expression following treatment with MECO or MECB was also observed. The downregulation of Sp1 by siRNA resulted in growth inhibition and a reduction of total poly (ADP-ribose) polymerase (PARP) expression. In addition, MECO significantly increased Bax expression levels and MECB increased Bak expression levels and decreased Mcl-1 expression levels. These results suggest that MECO and MECB inhibit cell growth and induce apoptosis via the Sp1 protein, indicating that MECO and MECB are useful bioactive materials and attractive drug candidates for oral cancer.

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