MMP-7 is upregulated by COX-2 and promotes proliferation and invasion of lung adenocarcinoma cells

Submitted: 17 August 2013
Accepted: 13 January 2014
Published: 18 February 2014
Abstract Views: 2604
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Matrix metalloproteinases (MMPs) have been implicated in a variety of pathophysiological conditions, of which MMP-7 is expressed by tumor cells of epithelial and mesenchymal origin. However, the function of MMP-7 in human lung adenocarcinoma (LAC) is unclear. In the present study the expression of MMP-7 in LAC was examined by immunohistochemical assay using a tissue microarray procedure. A loss-of-function experiment was performed to explore the effects and molecular mechanisms of lentiviral vector-mediated MMP-7 siRNA (siMMP-7) on cell proliferation and invasive potential in LAC A549 cells, measured by MTT and Transwell assays, respectively. It was found that, the expression of MMP-7 protein in LAC was significantly increased compared with that in adjacent non-cancerous tissues (ANCT) (76.0% vs 44.0%, P<0.001), and positively correlated with lymph node metastases of the tumor (P=0.014). Furthermore, targeted inhibition of cyclooxygenase-2 (COX-2) by siRNA downregulated the expression of MMP-7 and inhibited invasion of LAC cells, and knockdown of MMP-7 suppressed tumor proliferation and invasion in LAC cells. Taken together, our findings indicate that increased expression of MMP-7 is associated with lymph node metastasis and upregulated by COX-2, and promotes the tumorigenesis of LAC, suggesting that MMP-7 may be a potential therapeutic target for the treatment of cancer.

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Supporting Agencies

Shanghai Municipal Natural Science Foundation (No. 10ZR14249000.
D. Zheng, Shanghai Pulmonary Hospital, Tongji University School of Medicine,
Department of Medical Oncology

How to Cite

Zhang, J., Luo, J., Ni, J., Tang, L., Zhang, H., Zhang, L., … Zheng, D. (2014). MMP-7 is upregulated by COX-2 and promotes proliferation and invasion of lung adenocarcinoma cells. European Journal of Histochemistry, 58(1). https://doi.org/10.4081/ejh.2014.2262

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