Selaginella tamariscina extract suppresses TPA-induced invasion and metastasis through inhibition of MMP-9 in human nasopharyngeal carcinoma HONE-1 cells
1 School of Medicine, Chung Shan Medical University, Taichung, Taiwan
2 Department of Otolaryngology, Chung Shan Medical University Hospital, Taichung, Taiwan
3 School of Dentistry, Chung Shan Medical University, Taichung, Taiwan
4 Department of Dentistry, Chung Shan Medical University Hospital, Taichung, Taiwan
5 Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan
6 Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan
7 Department of Biochemistry, School of Medicine, Chung Shan Medical University, Taichung, Taiwan
8 Department of Otorhinolaryngology-Head and Neck Surgery, Changhua Christian Hospital, Changhua, Taiwan
9 Institute of Oral Sciences, Chung Shan Medical University, 110 Chien-Kuo N. Road, Section 1, Taichung, Taiwan
BMC Complementary and Alternative Medicine 2013, 13:234 doi:10.1186/1472-6882-13-234Published: 23 September 2013
Nasopharyngeal carcinoma (NPC) is known for its high incidence of neck lymph node metastasis, which represents poor prognosis. The present study aimed to examine the anti-metastatic properties of Selaginella tamariscina extract (STE) in human nasopharyngeal carcinoma HONE-1 cells in vitro.
Cell viability was examined by MTT assay, whereas cell motility was measured by invasive, migration and would healing assays. Real-time PCR, and promoter assays confirmed the inhibitory effects of STE on matrix metalloproteinase-9 (MMP-9) mRNA level in HONE-1 cells.
The STE inhibits 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced HONE-1 cell migration and invasion in a concentration-dependent manner. By zymographic and Western blot analyses, STE was shown to inhibit the activities and expression of MMP-9. Treatment of STE on TPA-induced HONE-1 cells inhibited MMP-9 expression and ERK1/2 phosphorylation without affecting JNK and p38 phosphorylation.
STE inhibits MMP-9 expression and HONE-1 cell metastasis. Its inhibitory effects may involve the Src/FAK/ERK 1/2 pathway. STE may have the potential of being an anti-metastatic agent against NPC.