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Resistance to caspa...
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Janson, VeronicaUmeå universitet,Klinisk kemi
(författare)
Resistance to caspase-8 and -9 fragments in a malignant pleural mesothelioma cell line with acquired cisplatin-resistance.
- Artikel/kapitelEngelska2010
Förlag, utgivningsår, omfång ...
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2010-09-23
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Nature Publishing Group,2010
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printrdacarrier
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LIBRIS-ID:oai:DiVA.org:umu-40650
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https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-40650URI
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https://doi.org/10.1038/cddis.2010.54DOI
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Språk:engelska
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Sammanfattning på:engelska
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Ämneskategori:art swepub-publicationtype
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Apoptotic cysteine-aspartate proteases (caspases) are essential for the progression and execution of apoptosis, and detection of caspase fragmentation or activity is often used as markers of apoptosis. Cisplatin (cis-diamminedichloroplatinum (II)) is a chemotherapeutic drug that is clinically used for the treatment of solid tumours. We compared a cisplatin-resistant pleural malignant mesothelioma cell line (P31res1.2) with its parental cell line (P31) regarding the consequences of in vitro acquired cisplatin-resistance on basal and cisplatin-induced (equitoxic and equiapoptotic cisplatin concentrations) caspase-3, -8 and -9 fragmentation and proteolytic activity. Acquisition of cisplatin-resistance resulted in basal fragmentation of caspase-8 and -9 without a concomitant increase in proteolytic activity, and there was an increased basal caspase-3/7 activity. Similarly, cisplatin-resistant non-small-cell lung cancer cells, H1299res, had increased caspase-3 and -9 content compared with the parental H1299 cells. In P31 cells, cisplatin exposure resulted in caspase-9-mediated caspase-3/7 activation, but in P31res1.2 cells the cisplatin-induced caspase-3/7 activation occurred before caspase-8 or -9 activation. We therefore concluded that in vitro acquisition of cisplatin-resistance rendered P31res1.2 cells resistant to caspase-8 and caspase-9 fragments and that cisplatin-induced, initiator-caspase independent caspase-3/7 activation was necessary to overcome this resistance. Finally, the results demonstrated that detection of cleaved caspase fragments alone might be insufficient as a marker of caspase activity and ensuing apoptosis induction.
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Johansson, AndersUmeå universitet,Institutionen för odontologi(Swepub:umu)anjo0002
(författare)
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Grankvist, KjellUmeå universitet,Klinisk kemi(Swepub:umu)kjgr0002
(författare)
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Umeå universitetKlinisk kemi
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:Cell death & disease: Nature Publishing Group1:9, s. e78-2041-4889
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