Gallic acid inhibits migration and invasion of SCC-4 human oral cancer cells through actions of NF-κB, Ras and matrix metalloproteinase-2 and -9
| Autor: | Kuang Chi Lai, Shu Wen Weng, Chao Lin Kuo, Jing Pin Lin, Yi Shih Ma, Jing Gung Chung |
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| Rok vydání: | 2014 |
| Předmět: |
Cancer Research
RHOA Cell Survival Cell Cell Movement Cell Line Tumor Gallic Acid medicine Humans Neoplasm Invasiveness Matrigel Oncogene biology NF-kappa B Cell migration General Medicine Cell cycle Protein Transport stomatognathic diseases medicine.anatomical_structure Matrix Metalloproteinase 9 Oncology Apoptosis Cancer cell Immunology ras Proteins Cancer research biology.protein Matrix Metalloproteinase 2 Mouth Neoplasms Signal Transduction |
| Zdroj: | Oncology Reports. 32:355-361 |
| ISSN: | 1791-2431 1021-335X |
| Popis: | Oral cancer is one of the major causes of mortality in humans and squamous cell carcinoma is the most common type of oral cancer. Gallic acid (GA) is a natural product that induces cell death through cell cycle arrest and induction of apoptosis. There is no available information on whether GA affects cell migration and invasion of human oral cancer cells. We determined if GA inhibited migration and invasion of SCC-4 (human squamous cell carcinoma) human oral cancer cells. GA significantly inhibited migration and invasion of SCC-4 cells based on results from the wound healing assay and Matrigel Cell Migration Assay and Invasion System. We also showed that GA significantly inhibited matrix metalloproteinase (MMP)-2 and MMP-9 activity. GA reduced protein levels of FAK, MEKK3, p-PERK, p-p38, p-JNK1/2, p-ERK1/2, SOS1, RhoA, Ras, PKC, p-AKT(Thr308), PI3K, NF-κB p65, MMP-2 and MMP-9 in SCC-4 cells. Translocation of NF-κB and RhoA from the cytosol to the nucleus was reduced by GA in SCC-4 cells. In summary, GA inhibits migration and invasion of SCC-4 cells by inhibiting NF-κB expression causing suppression of MMP-2 and MMP-9 activity. GA may have potential as a therapeutic agent for the treatment of oral cancer. |
| Databáze: | OpenAIRE |
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