| Autor: |
Schempp CM; Department of Dermatology, University of Freiburg, Hauptstrasse 7, D-79104, Freiburg, Germany. schempp@haut.ukl.uni-freiburg.de, Simon-Haarhaus B, Termeer CC, Simon JC |
| Jazyk: |
angličtina |
| Zdroj: |
FEBS letters [FEBS Lett] 2001 Mar 23; Vol. 493 (1), pp. 26-30. |
| DOI: |
10.1016/s0014-5793(01)02268-2 |
| Abstrakt: |
Hypericin (HYP) is a photosensitizing pigment from Hypericum perforatum that displays cytotoxic effects in neoplastic cell lines. Therefore, HYP is presently under consideration as a new anticancer drug in photodynamic therapy. Here, we investigated the mechanism of action of HYP photo-induced apoptosis of Jurkat cells compared to the cytostatic drug paclitaxel (PXL). Both photoactivated HYP and PXL similarly increased the activity of caspase-8 and caspase-3, and drug-induced apoptosis of Jurkat cells was completely blocked by inhibitors of caspase-8 (Z-IETD-FMK) and caspase-3 (Z-DEVD-FMK). The involvement of death receptors was analyzed using neutralizing monoclonal antibodies against Fas (SM1/23), FasL (NOK-2) and TNF-R1 (MAB225), and a polyclonal rabbit anti-human TNF-related apoptosis-inducing ligand (TRAIL) antiserum. TRAIL antibody blocked TRAIL-induced and HYP photo-induced, but not PXL-induced apoptosis of Jurkat cells. In contrast, PXL-induced, but not HYP-induced apoptosis was blocked by the SM1/23 and NOK-2 antibodies. Anti-TNF-R1 antibody had no effect. These findings suggest that HYP photo-induced apoptosis of Jurkat cells is mediated in part by the TRAIL/TRAIL-receptor system and subsequent activation of upstream caspases. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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