liu.seSearch for publications in DiVA
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
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..
Linköping University, Department of Medical and Health Sciences, Clinical Pharmacology. Linköping University, Faculty of Health Sciences. (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..
Show others and affiliations
2011 (English)In: Cancer Letters, ISSN 0304-3835, E-ISSN 1872-7980, Vol. 307, no 2, 119-23 p.Article in journal (Refereed) 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.

Place, publisher, year, edition, pages
2011. Vol. 307, no 2, 119-23 p.
Keyword [en]
Lysosomes, Endocytosis, Cancer therapy, Oxidative stress, Thioredoxin reductase
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-69261DOI: 10.1016/j.canlet.2011.03.023PubMedID: 21492999OAI: oai:DiVA.org:liu-69261DiVA: diva2:425070
Available from: 2011-06-20 Created: 2011-06-20 Last updated: 2017-12-11

Open Access in DiVA

No full text

Other links

Publisher's full textPubMed

Authority records BETA

Kurz, TinoBrunk, Ulf T

Search in DiVA

By author/editor
Kurz, TinoBrunk, Ulf T
By organisation
Clinical PharmacologyFaculty of Health Sciences
In the same journal
Cancer Letters
Medical and Health Sciences

Search outside of DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 65 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf