Induction of Urokinase-type Plasminogen Activator by Sodium Salicylate in a Glioblastoma Cell Strain

Maja Matulić* and Branko Brdar

Department of Molecular Biology, Division of Biology, Faculty of Science, University of Zagreb, Horvatovac 102A, HR-10000 Zagreb, Croatia

Article history:

Received June 30, 2000
Accepted October 26, 2000

Key words:

urokinase, uPA promoter, sodium salicylate, NF-κB, gadd45, glioblastoma cell strain


Urokinase-type plasminogen activator (uPA) is an extracellular protease involved in many physiological and patological processes. In this paper its induction by sodium salicylate (NaSal) in A1235 glioblastoma cell strain is described. Maximum uPA induction was observed 24–36 h after NaSal treatment and levels of enzyme produced were 5–7 times as high as those of untreated control. uPA induction was based on the uPA promoter activation – both, 2.2kb and 5.5kb uPA promoters, containing single and two AP-1/PEA3 binding sites, respectively, were activated. NaSal also caused substantial cell growth inhibition and cell morphology changes. Curcumin and pyrrolidine dithiocarbamate (PDTC), NF-κB inhibitors, did not abrogate NaSal induced uPA promoter activity, nor induced uPA, suggesting that NF-κB is not involved in this uPA induction. This observation was also confirmed by immunoblot analysis on IκB. Aspirin (acetylsalicylate) also activated uPA promoter and induced uPA production. The results in this paper suggest that NaSal induced uPA production is based on the uPA promoter activation through an NF-κB independent pathway.


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