Antimetastatic potentials of salvianolic acid A on oral squamous cell carcinoma by targeting MMP‐2 and the c‐Raf/MEK/ERK pathway

The metastasis of oral squamous cell carcinoma (OSCC) is one of the most important causes of cancer‐related deaths. Thus, various therapeutic strategies have been developed to prevent the metastasis of OSCC. Salvianolic acid A (SAA), a traditional Chinese medicine, has antithrombosis, antiplatelet,...

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Published in:Environmental toxicology 2018-05, Vol.33 (5), p.545-554
Main Authors: Fang, Chih‐Yuan, Wu, Ching‐Zong, Chen, Pei‐Ni, Chang, Yu‐Chao, Chuang, Chun‐Yi, Lai, Chih‐Ting, Yang, Shun‐Fa, Tsai, Lo‐Lin
Format: Article
Language:English
Subjects:
Acids
Anticancer properties
Antitumour agents
Cancer
Cell adhesion & migration
Cell migration
Cells
Extracellular signal-regulated kinase
Herbal medicine
invasion
Metabolic pathways
Metastases
Metastasis
MMP‐2
Molecular modelling
Neoplasms
Oral cancer
Oral squamous cell carcinoma
Proteins
Raf protein
salvianolic acid A
Squamous cell carcinoma
Traditional Chinese medicine
Western blotting
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Summary:The metastasis of oral squamous cell carcinoma (OSCC) is one of the most important causes of cancer‐related deaths. Thus, various therapeutic strategies have been developed to prevent the metastasis of OSCC. Salvianolic acid A (SAA), a traditional Chinese medicine, has antithrombosis, antiplatelet, anti‐inflammation, and antitumor activities. Here, we provide molecular evidence indicating that SAA exerts its antimetastatic effects by markedly inhibiting the invasion and migration of oral squamous SCC‐9 and SCC‐25 cells. SCC‐9 and SCC‐25 cells were treated with various concentrations of SAA to further investigate the precise involvement of SAA in cancer metastasis. The results of zymography, and Western blotting indicated that SAA treatment may decrease matrix metallopoteinase‐2 (MMP‐2) expression. SAA also inhibited p‐c‐Raf, p‐MEK1/2, and p‐ERK1/2 protein expression. In addition, treating SCC‐9 cells with U0126, a MEK‐specific inhibitor, decreased MMP‐2 expression and concomitantly inhibited cell migration. Our findings suggested that SAA inhibits the invasion and migration of OSCC by inhibiting the c‐Raf/MEK/ERK pathways that control MMP‐2 expression. Our findings provide new insights into the molecular mechanisms that underlie the antimetastatic effect of SAA and are thus valuable for the development of treatment strategies for metastatic OSCC.
ISSN:1520-4081
1522-7278
DOI:10.1002/tox.22542