Collagen XVI induces expression of MMP9 via modulation of AP-1 transcription factors and facilitates invasion of oral squamous cell carcinoma.

Collagen XVI induces expression of MMP9 via modulation of AP-1 transcription factors and facilitates invasion of oral squamous cell carcinoma.

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Collagen XVI belongs to the family of fibril-associated collagens with interrupted triple helices (FACIT).It is overexpressed during the progression of oral squamous cell carcinoma (OSCC).The present data show a strong collagen XVI-dependent induction of MMP9 and an increase in OSCC cell invasion.We found activated integrin-linked kinase (ILK) in a complex with kindlin-1 and activation of protein kinase B (PKB/Akt) to be responsible for MMP9 induction.

Inhibition of hp 15-ef1005ds the formation of focal adhesions reduced MMP9 expression.Moreover, collagen XVI overexpressing OSCC cell clones (COLXVI cell clones) transfected with vectors containing different MMP9 promoter fragments adjacent to a luciferase reporter revealed an increase in luciferase signal dependent on AP-1 binding sites.Deletion of the AP-1 binding site 98 bp upstream of the reported transcription start site and inhibition of AP-1 ashley stewart outlet with Tanshinone IIA resulted in decreased MMP9 expression.The AP-1 subunit JunB showed differential expression between COLXVI cell clones and mock control cells.

Additionally, mass spectrometric analysis of immunoprecipitates revealed that c-Fos interacted strongly with dyskerin in COLXVI cell clones compared to mock controls.