COX-2-dependent PGE(2) acts as a growth factor in mycosis fungoides (MF)

Katharina Luise Maria Kopp, C S Kauczok, Britt Thyssing Lauenborg, Thorbjørn Frej Krejsgaard, K W Eriksen, Q Zhang, M A Wasik, C Geisler, E Ralfkiaer, J C Becker, Niels Ødum, Alex Le Woetmann Danielsen

39 Citationer (Scopus)


Cancer often originates from a site of persistent inflammation, and the mechanisms turning chronic inflammation into a driving force of carcinogenesis are intensely investigated. Cyclooxygenase-2 (COX-2) is an inducible key modulator of inflammation that carries out the rate-limiting step in prostaglandin synthesis. Aberrant COX-2 expression and prostaglandin E(2) (PGE(2)) production have been implicated in tumorigenesis. In this study we show that COX-2 is ectopically expressed in malignant T-cell lines from patients with cutaneous T-cell lymphoma (CTCL) as well as in situ in lymphocytic cells in 21 out of 22 patients suffering from mycosis fungoides (MF) in plaque or tumor stage. COX-2 is not expressed in lymphocytes of 11 patients with patch-stage MF, whereas sporadic COX-2 staining of stromal cells is observed in the majority of patients. COX-2 expression correlates with a constitutive production of PGE(2) in malignant T cells in vitro. These cells express prostaglandin receptors EP3 and EP4 and the receptor antagonist as well as small interfering RNA (siRNA) directed against COX-2, and specific COX-2 inhibitors strongly reduce their spontaneous proliferation. In conclusion, our data indicate that COX-2 mediated PGE(2) exerts an effect as a tumor growth factor in MF.
Udgave nummer6
Sider (fra-til)1179-85
Antal sider7
StatusUdgivet - 1 jun. 2010


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