Aspirin inhibits matrix metalloproteinase-2 activity, increases E-cadherin production, and inhibits in Vitro invasion of tumor cells
Journal
Biochemical and Biophysical Research Communications
Journal Volume
282
Journal Issue
3
Pages
671-677
Date Issued
2001
Author(s)
Abstract
Aspirin (acetylsalicylic acid) is a widely used anti-inflammatory drug. Recently, aspirin was shown to reduce the risk of development of cancer and mortality from it. Tumor metastasis is the most important cause of cancer death. The aim of the present study was to investigate if aspirin affects the invasion of cancer cells. Matrix metalloproteinases (MMPs) and cell adhesion molecules play important roles in the modulation of tumor invasion. Gelatin-based zymography assay showed that aspirin inhibited MMP-2 activity of SK-Hep-1 cancer cells. Matrigel-based chemoinvasion assay showed that aspirin inhibited in vitro invasion of SK-Hep-1 cancer cells. Aspirin treatment also increased the production of the cell adhesion molecule, E-cadherin, in Hep G2 cancer cells. Aspirin is a cyclooxygenase (COX) inhibitor. Treatment of cells with another COX inhibitor, sulindac, also inhibited MMP-2 activity and increased E-cadherin production of cells. These results indicate that aspirin can modulate both MMP-2 and E-cadherin production and therein may possess antimetastatic effect. ? 2001 Academic Press.
SDGs
Other Subjects
acetylsalicylic acid; antiinflammatory agent; gelatin; gelatinase A; matrigel; sulindac; uvomorulin; article; cancer invasion; cancer mortality; cell invasion; cell migration; cell strain HepG2; enzyme activity; enzyme degradation; enzyme inhibition; epithelium cell; extracellular matrix; human; human cell; priority journal; tumor cell culture; tumor growth
Publisher
Academic Press Inc.
Type
journal article