Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-5810
Full metadata record
DC FieldValueLanguage
dc.contributor.authorKiweler, Nicole-
dc.contributor.authorWünsch, Désirée-
dc.contributor.authorWirth, Matthias-
dc.contributor.authorMahendrarajah, Nisintha-
dc.contributor.authorSchneider, Günter-
dc.contributor.authorStauber, Roland-
dc.contributor.authorBrenner, Walburgis-
dc.contributor.authorButter, Falk-
dc.contributor.authorKrämer, Oliver-
dc.date.accessioned2021-05-18T10:17:42Z-
dc.date.available2021-05-18T10:17:42Z-
dc.date.issued2020-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/5819-
dc.description.abstractPURPOSE We set out to determine whether clinically tested epigenetic drugs against class I histone deacetylases (HDACs) affect hallmarks of the metastatic process. METHODS We treated permanent and primary renal, lung, and breast cancer cells with the class I histone deacetylase inhibitors (HDACi) entinostat (MS-275) and valproic acid (VPA), the replicative stress inducer hydroxyurea (HU), the DNA-damaging agent cis-platinum (L-OHP), and the cytokine transforming growth factor-β (TGFβ). We used proteomics, quantitative PCR, immunoblot, single cell DNA damage assays, and flow cytometry to analyze cell fate after drug exposure. RESULTS We show that HDACi interfere with DNA repair protein expression and trigger DNA damage and apoptosis alone and in combination with established chemotherapeutics. Furthermore, HDACi disrupt the balance of cell adhesion protein expression and abrogate TGFβ-induced cellular plasticity of transformed cells. CONCLUSION HDACi suppress the epithelial–mesenchymal transition (EMT) and compromise the DNA integrity of cancer cells. These data encourage further testing of HDACi against tumor cells.en_GB
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleHistone deacetylase inhibitors dysregulate DNA repair proteins and antagonize metastasis-associated processesen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-5810-
jgu.type.contenttypeScientific articlede
jgu.type.dinitypearticleen_GB
jgu.type.versionPublished versionde
jgu.type.resourceTextde
jgu.organisation.departmentFB 04 Medizinde
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleJournal of cancer research and clinical oncologyde
jgu.journal.volume146de
jgu.pages.start343de
jgu.pages.end356de
jgu.publisher.year2020-
jgu.publisher.nameSpringerde
jgu.publisher.placeBerlin u.a.de
jgu.publisher.urihttps://doi.org/10.1007/s00432-019-03118-4de
jgu.publisher.issn1432-1335de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
jgu.publisher.doi10.1007/s00432-019-03118-4
jgu.organisation.rorhttps://ror.org/023b0x485
Appears in collections:JGU-Publikationen

Files in This Item:
  File Description SizeFormat
Thumbnail
kiweler_nicole-histone_deacet-20210422211427156.pdf3.54 MBAdobe PDFView/Open