Home Bratislava Medical Journal 2015 Bratislava Medical Journal Vol.116, No.4, p.227-232, 2015

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Published Monthly, in English
Founded: 1919
ISSN 0006-9248
(E)ISSN 1336-0345

Impact factor 1.564


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Bratislava Medical Journal Vol.116, No.4, p.227-232, 2015

Title: Crosstalk between possible cytostatic and antiinflammatory potential of ketoprofen in the treatment of culture of colon and cervix cancer cell lines
Author: I. Damnjanovic, S. Najman, S. Stojanovic, D. Stojanovic, A. Veljkovic, H. Kocic, T. Langerholc, Z. Damnjanovic, S. Pesic

Abstract: Objectives: The aim of this study was to test the cytostatic potential of ketoprofen in the in vitro treatment of cells derived from colon and cervix cancer.
Background: NF-κB and cyclooxygenase can have a role in different stages of the development and progression of cancer. In recent years, special attention has been paid to the possible cytostatic potential of nonsteroidal anti-inflammatory drugs. There are no published data on the use of ketoprofen in pharmacotherapy of the colon and cervical carcinoma.
Methods: We examined the effect of ketoprofen alone or in combination with cisplatin and 5-fluorouracil on proliferation of the two cell lines, HeLa (human cervical carcinoma cells) and Caco-2 (human colon cancer cells) by MTT test. Measurement of the level of NF-κB was also performed in the cells of both cell lines.
Results: The results of present study have shown that at least one of the mechanisms of antiproliferating and/or cytostatic effects of different concentrations of ketoprofen on Caco-2 and HeLa cells could include the transcription factor NF-κB.
Conclusions: Since this transcription factor is controlled by the altered expression of COX-2, the inhibition of this enzyme by ketoprofen may represent a significant step in synergistic cascade of the therapy and prevention of colon and cervical cancer (Tab. 4, Ref. 31).

Keywords: ketoprofen, cytostatic potential, HeLa cells, Caco-2 cells, NF-κB, cyclooxygenase.
Year: 2015, Volume: 116, Issue: 4 Page From: 227, Page To: 232

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