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Kalopanaxsaponin A inhibits the invasion of human oral squamous cell carcinoma by reducing metalloproteinase-9 mRNA stability and protein trafficking

Title
 Kalopanaxsaponin A inhibits the invasion of human oral squamous cell carcinoma by reducing metalloproteinase-9 mRNA stability and protein trafficking 
Authors
 Young Sun Hwang ; Kwang-Kyun Park ; Won-Yoon Chung 
Issue Date
2012
Journal Title
 Biological & Pharmaceutical Bulletin 
ISSN
 0918-6158 
Citation
 Biological & Pharmaceutical Bulletin, Vol.35(3) : 289~300, 2012 
Abstract
An inability to control cancer cell invasion and metastasis is the leading cause of death in patients with cancer. The present study was performed to determine the anti-invasive effect of Kalopanaxsaponin A (KPS-A) on matrix metalloproteinase-9 (MMP-9)-meidated invasion in phorbol 12-myristate 13-acetate (PMA)-stimulated human oral squamous cell carcinoma (OSCC) cells and a murine xenograft model of human OSCC. KPS-A, isolated from Kalopanax pictus, inhibited PMA-induced proliferation and invasion as well as PMA-induced MMP-9 expression and secretion at non-cytotoxic doses. KPS-A treatment reduced the stability of PMA-induced MMP-9 mRNA and inhibited the PMA-induced cytoplasmic translocation of HuR. In PMA-treated cells, KPS-A treatment resulted in the intracellular accumulation of MMP-9 and suppressed Ras-associated binding 1A (Rab1A) expression. KPS-A treatment suppressed PMA-induced phosphorylation of extracellular signal regulated kinase (ERK)1/2 and Akt. Furthermore, the oral administration of KPS-A led to substantial inhibition of tumor growth and the expression of proliferating cell nuclear antigen (PCNA), MMP-9, tissue inhibitor of metalloproteinase-1 (TIMP-1), HuR, and Rab1A in the tumor tissues of mice inoculated with YD-10B OSCC cells. Collectively, KPS-A inhibits the invasiveness of oral cancer by reducing HuR-mediated MMP-9 mRNA stability and Rab1A-mediated MMP-9 secretion via ERK1/2 and phosphatidylinositide 3-kinase (PI3K)/Akt. Therefore, KPS-A is a promising anti-invasive agent.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/89719
Appears in Collections:
1. 연구논문 > 5. Research Institutes > Oral Cancer Research Institute
1. 연구논문 > 2. College of Dentistry > Dept. of Oral Biology
Yonsei Authors
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