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Increase of MMP‐13 expression in multi‐stage oral carcinogenesis and epigallocatechin‐3‐gallate suppress MMP‐13 expression
Author(s) -
Chiang WC,
Wong YK,
Lin SC,
Chang KW,
Liu CJ
Publication year - 2006
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/j.1601-0825.2005.01151.x
Subject(s) - matrix metalloproteinase , epigallocatechin gallate , collagenase , immunohistochemistry , carcinogenesis , cancer research , extracellular matrix , gelatinase a , tumor progression , messenger rna , pathology , cell , zymography , chemistry , biology , cancer , medicine , enzyme , polyphenol , gene , biochemistry , antioxidant
Background: Matrix metalloproteinases (MMPs) play pivotal roles in tumor progression. MMP‐13 (collagenase‐3) digests collagen and other extracellular components. Materials and Methods: Reverse transcriptase‐polymerase chain reaction (RT‐PCR), immunohistochemistry and zymograph were used to study the roles of MMP‐13 during the neoplastic process of oral squamous cell carcinoma (OSCC). Results: Increase of MMP‐13 mRNA and protein expression in OSCC cell lines relative to cultivated normal oral keratinocytes was found. MMP‐13 mRNA expression in OSCC was significantly higher than in non‐cancerous match tissue (NCMT) in 36 tissue pairs. Esophageal squamous cell carcinoma also exhibited high MMP‐13 mRNA expression. The percentage of OSCC exhibiting strong MMP‐13 immunoreactivity was significantly higher than pre‐invasive lesion and NCMT. Treatment with >5 μ m epigallocatechin‐3‐gallate (EGCG) to OEC‐M1 cells suppressed the expression and activity of MMP‐13. Conclusion: MMP‐13 could be a potential tumor marker for OSCC. The effects of EGCG in tumor inhibition may act partially through the modulation of MMP‐13.