Sp1 regulates cathepsin B transcription and invasiveness in murine B16 melanoma cells.

Background: Increased expression of cathepsin B contributes to extracellular matrix degradation and invasion in cancer. Cathepsin B expression is under transcriptional control in murine melanomas and the major promoter contains potential binding sites for the Sp1 transcription factor.

Materials And Methods: Murine melanoma cells transfected with an Sp1 expression plasmid or its control were used in Matrigel invasion and cell motility assays in the presence or absence of the cathepsin B inhibitor, CA-074Me.

Results: Transfection of B16F1 cells with the Sp1 expression plasmid resulted in a 2.5- to 5.3 -fold increase in cathepsin B specific activity and a 4.8- to 5.5-fold increase in invasiveness over the control, but had no effect on the movement of cells across an uncoated membrane. CA-074Me treatment resulted in significantly reduced Matrigel invasion without affecting cell motility.

Conclusion: Sp1 can regulate the capacity of B16F1 cells to degrade a reconstituted extracellular matrix in part by regulating cathepsin B expression.