Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-810
Full metadata record
DC FieldValueLanguage
dc.contributor.authorWiench, Benjamin-
dc.contributor.authorEichhorn, Tolga-
dc.contributor.authorPaulsen, Malte-
dc.contributor.authorEfferth, Thomas-
dc.date.accessioned2013-01-31T15:38:06Z-
dc.date.available2013-01-31T16:38:06Z-
dc.date.issued2012-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/812-
dc.description.abstractChemotherapy is a mainstay of cancer treatment. Due to increased drug resistance and the severe side effects of currently used therapeutics, new candidate compounds are required for improvement of therapy success. Shikonin, a natural naphthoquinone, was used in traditional Chinese medicine for the treatment of different inflammatory diseases and recent studies revealed the anticancer activities of shikonin. We found that shikonin has strong cytotoxic effects on 15 cancer cell lines, including multidrug-resistant cell lines. Transcriptome-wide mRNA expression studies showed that shikonin induced genetic pathways regulating cell cycle, mitochondrial function, levels of reactive oxygen species, and cytoskeletal formation. Taking advantage of the inherent fluorescence of shikonin, we analyzed its uptake and distribution in live cells with high spatial and temporal resolution using flow cytometry and confocal microscopy. Shikonin was specifically accumulated in the mitochondria, and this accumulation was associated with a shikonin-dependent deregulation of cellular Ca(2+) and ROS levels. This deregulation led to a breakdown of the mitochondrial membrane potential, dysfunction of microtubules, cell-cycle arrest, and ultimately induction of apoptosis. Seeing as both the metabolism and the structure of mitochondria show marked differences between cancer cells and normal cells, shikonin is a promising candidate for the next generation of chemotherapy.en_GB
dc.description.sponsorshipDFG, Open Access-Publizieren Universität Mainz / Universitätsmedizin-
dc.language.isoeng-
dc.rightsCC BYde_DE
dc.rights.urihttps://creativecommons.org/licenses/by/3.0/-
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleShikonin directly targets mitochondria and causes mitochondrial dysfunction in cancer cellsen_GB
dc.typeZeitschriftenaufsatzde_DE
dc.identifier.urnurn:nbn:de:hebis:77-32616-
dc.identifier.doihttp://doi.org/10.25358/openscience-810-
jgu.type.dinitypearticle-
jgu.type.versionPublished versionen_GB
jgu.type.resourceText-
jgu.organisation.departmentFB 09 Chemie, Pharmazie u. Geowissensch.-
jgu.organisation.number7950-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleEvidence-based complementary and alternative medicine-
jgu.journal.volume9-
jgu.pages.start1-
jgu.pages.end15-
jgu.publisher.year2012-
jgu.publisher.nameHindawi-
jgu.publisher.placeNew York, NY-
jgu.publisher.urihttp://dx.doi.org/10.1155/2012/726025-
jgu.publisher.issn1741-427X-
jgu.organisation.placeMainz-
jgu.subject.ddccode610-
opus.date.accessioned2013-01-31T15:38:06Z-
opus.date.modified2019-08-16T09:34:10Z-
opus.date.available2013-01-31T16:38:06-
opus.organisation.stringFB 09: Chemie, Pharmazie und Geowissenschaften: Institut für Pharmaziede_DE
opus.identifier.opusid3261-
opus.institute.number0908-
opus.metadataonlyfalse-
opus.type.contenttypeForschungsberichtde_DE
opus.type.contenttypeResearch Reporten_GB
opus.affiliatedEfferth, Thomas-
jgu.publisher.doi10.1155/2012/726025
jgu.organisation.rorhttps://ror.org/023b0x485
Appears in collections:JGU-Publikationen

Files in This Item:
  File Description SizeFormat
Thumbnail
3261.pdf3.28 MBAdobe PDFView/Open