Shikonin Directly Targets Mitochondria and Causes Mitochondrial Dysfunction in Cancer Cells
- Publication type:
- Journal article
- Metadata:
-
- Autoren
- Benjamin Wiench
- Tolga Eichhorn
- Malte Paulsen
- Thomas Efferth
- Autoren-URL
- https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=fis-test-1&SrcAuth=WosAPI&KeyUT=WOS:000310287400001&DestLinkType=FullRecord&DestApp=WOS_CPL
- DOI
- 10.1155/2012/726025
- eISSN
- 1741-4288
- Externe Identifier
- Clarivate Analytics Document Solution ID: 026NU
- PubMed Identifier: 23118796
- ISSN
- 1741-427X
- Zeitschrift
- EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE
- Artikelnummer
- ARTN 726025
- Datum der Veröffentlichung
- 2012
- Status
- Published
- Titel
- Shikonin Directly Targets Mitochondria and Causes Mitochondrial Dysfunction in Cancer Cells
- Sub types
- Article
- Ausgabe der Zeitschrift
- 2012
Data source: Web of Science (Lite)
- Other metadata sources:
-
- Abstract
- <jats:p>Chemotherapy 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<jats:sup>2+</jats:sup>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.</jats:p>
- Autoren
- Benjamin Wiench
- Tolga Eichhorn
- Malte Paulsen
- Thomas Efferth
- DOI
- 10.1155/2012/726025
- eISSN
- 1741-4288
- ISSN
- 1741-427X
- Zeitschrift
- Evidence-Based Complementary and Alternative Medicine
- Sprache
- en
- Paginierung
- 1 - 15
- Datum der Veröffentlichung
- 2012
- Status
- Published
- Herausgeber
- Hindawi Limited
- Herausgeber URL
- http://dx.doi.org/10.1155/2012/726025
- Datum der Datenerfassung
- 2024
- Titel
- Shikonin Directly Targets Mitochondria and Causes Mitochondrial Dysfunction in Cancer Cells
- Ausgabe der Zeitschrift
- 2012
Data source: Crossref
- Abstract
- Chemotherapy 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.
- Addresses
- Department of Pharmaceutical Biology, Institute of Pharmacy and Biochemistry, Johannes Gutenberg University, Staudinger Weg 5, 55128 Mainz, Germany.
- Autoren
- Benjamin Wiench
- Tolga Eichhorn
- Malte Paulsen
- Thomas Efferth
- Thomas Efferth
- DOI
- 10.1155/2012/726025
- eISSN
- 1741-4288
- Externe Identifier
- PubMed Identifier: 23118796
- PubMed Central ID: PMC3478753
- Open access
- true
- ISSN
- 1741-427X
- Zeitschrift
- Evidence-based complementary and alternative medicine : eCAM
- Sprache
- eng
- Medium
- Print-Electronic
- Online publication date
- 2012
- Open access status
- Open Access
- Paginierung
- 726025
- Datum der Veröffentlichung
- 2012
- Status
- Published
- Publisher licence
- CC BY
- Datum der Datenerfassung
- 2012
- Titel
- Shikonin directly targets mitochondria and causes mitochondrial dysfunction in cancer cells.
- Sub types
- research-article
- Journal Article
- Ausgabe der Zeitschrift
- 2012
Files
https://downloads.hindawi.com/journals/ecam/2012/726025.pdf https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23118796/pdf/?tool=EBI https://europepmc.org/articles/PMC3478753?pdf=render
Data source: Europe PubMed Central
- Abstract
- Chemotherapy 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.
- Date of acceptance
- 2012
- Autoren
- Benjamin Wiench
- Tolga Eichhorn
- Malte Paulsen
- Thomas Efferth
- Autoren-URL
- https://www.ncbi.nlm.nih.gov/pubmed/23118796
- DOI
- 10.1155/2012/726025
- eISSN
- 1741-4288
- Externe Identifier
- PubMed Central ID: PMC3478753
- Zeitschrift
- Evid Based Complement Alternat Med
- Sprache
- eng
- Country
- United States
- Paginierung
- 726025
- Datum der Veröffentlichung
- 2012
- Status
- Published
- Datum, an dem der Datensatz öffentlich gemacht wurde
- 2012
- Titel
- Shikonin directly targets mitochondria and causes mitochondrial dysfunction in cancer cells.
- Sub types
- Journal Article
- Ausgabe der Zeitschrift
- 2012
Data source: PubMed
- Author's licence
- CC-BY
- Autoren
- Benjamin Wiench
- Tolga Eichhorn
- Malte Paulsen
- Thomas Efferth
- Hosting institution
- Universitätsbibliothek Mainz
- Sammlungen
- JGU-Publikationen
- Resource version
- Published version
- URN
- urn:nbn:de:hebis:77-32616
- DOI
- 10.1155/2012/726025
- Funding acknowledgements
- DFG, Open Access-Publizieren Universität Mainz / Universitätsmedizin
- File(s) embargoed
- false
- Open access
- true
- ISSN
- 1741-427X
- Zeitschrift
- Evidence-based complementary and alternative medicine
- Schlüsselwörter
- 610 Medizin
- 610 Medical sciences
- Sprache
- eng
- Open access status
- Open Access
- Paginierung
- 1 - 15
- Datum der Veröffentlichung
- 2012
- Public URL
- https://openscience.ub.uni-mainz.de/handle/20.500.12030/812
- Herausgeber
- Hindawi
- Herausgeber URL
- http://dx.doi.org/10.1155/2012/726025
- Datum der Datenerfassung
- 2013
- Datum, an dem der Datensatz öffentlich gemacht wurde
- 2013
- Zugang
- Public
- Titel
- Shikonin directly targets mitochondria and causes mitochondrial dysfunction in cancer cells
- Ausgabe der Zeitschrift
- 9
Files
3261.pdf
Data source: OPENSCIENCE.UB
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