Author: Nilsonne, Gustav; Sun, Xiaojuan; Nyström, Christina; Rundlöf, Anna-Klara; Potamitou Fernandes, Aristi; Björnstedt, Mikael; Dobra, Katalin
Department: Inst för laboratoriemedicin / Dept of Laboratory Medicine
Abstract
Malignant mesothelioma cells differentiate into sarcomatoid or epithelioid
phenotypes. The sarcomatoid cell type is more resistant to chemotherapy and yields a
worse prognosis. We have investigated whether selenite alone and in combination with
doxorubicin induced apoptosis in variously differentiated mesothelioma cells. Selenite in
concentrations that could potentially be administered to patients strongly inhibited the
growth of the sarcomatoid mesothelioma cells (IC 50 = 7.5 µM), whereas epithelioid
cells were more sensitive to doxorubicin. Benign mesothelial cells remained largely
unaffected. Selenite potentiates doxorubicin treatment.. Apoptosis was the dominating
mode of cell death. The toxicity of selenite was mediated by oxidative stress.
Furthermore the activity of the thioredoxin system was directly dependent on the
concentration of selenite. This offers a possible mechanism of action of selenite
treatment. Our findings suggest that selenite is a promising new drug for the treatment of
malignant mesothelioma.
Institution: Department of Laboratory Medicine, Karolinska University Hospital, F-46, Karolinska Institutet, S-141 86 Huddinge, Stockholm, Sweden.
Citation: Nilsonne G, Sun X, Nyström C, Rundlöf A-K, Fernandes A, Björnstedt M, Dobra K. Selenite induces apoptosis in sarcomatoid malignant mesothelioma cells through oxidative stress. Free Radical Biology and Medicine. 2006 41(6):874-85. doi: 10.1016/j.freeradbiomed.2006.04.031
Publishing journal: Free Radical Biology and Medicine
Eprint status: Peer Reviewed
Version: Accepted
Issue date: 2021-02-08
Sponsorship:
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Cancer- och allergifonden
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Svenska läkaresällskapet
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Hjärt-lungfonden
Rights:
Article is made available in accordance with the publisher's policy and may be subject to copyright law. Please refer to the publisher's site for terms of use.
Publication year: 2006