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Ascorbate and endocytosed Motexafin gadolinium induce lysosomal rupture.
Division of Biochemistry, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, 171 77 Stockholm, Sweden; Institute for Clinical Cytobiology and Cytopathology, Philipps-Universität, 35037 Marburg, Germany..
Linköpings universitet, Institutionen för medicin och hälsa, Klinisk farmakologi. Linköpings universitet, Hälsouniversitetet. (Medicin)
Division of Biochemistry, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, 171 77 Stockholm, Sweden.
Institute for Clinical Cytobiology and Cytopathology, Philipps-Universität, 35037 Marburg, Germany..
Vise andre og tillknytning
2011 (engelsk)Inngår i: Cancer Letters, ISSN 0304-3835, E-ISSN 1872-7980, Vol. 307, nr 2, s. 119-23Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Motexafin gadolinium (MGd) sensitizes malignant cells to ionizing radiation, although the underlying mechanisms for uptake and sensitization are both unclear. Here we show that MGd is endocytosed by the clathrin-dependent pathway with ensuing lysosomal membrane permeabilization, most likely via formation of reactive oxygen species involving redox-active metabolites, such as ascorbate. We propose that subsequent apoptosis is a synergistic effect of irradiation and high MGd concentrations in malignant cells due to their pronounced endocytic activity. The results provide novel insights into the mode of action of this promising anti-cancer drug, which is currently under clinical trials.

sted, utgiver, år, opplag, sider
2011. Vol. 307, nr 2, s. 119-23
Emneord [en]
Lysosomes, Endocytosis, Cancer therapy, Oxidative stress, Thioredoxin reductase
HSV kategori
Identifikatorer
URN: urn:nbn:se:liu:diva-69261DOI: 10.1016/j.canlet.2011.03.023PubMedID: 21492999OAI: oai:DiVA.org:liu-69261DiVA, id: diva2:425070
Tilgjengelig fra: 2011-06-20 Laget: 2011-06-20 Sist oppdatert: 2017-12-11

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