Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-5928
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dc.contributor.authorMarkowitsch, Sascha D.-
dc.contributor.authorJuetter, Kira M.-
dc.contributor.authorSchupp, Patricia-
dc.contributor.authorHauschulte, Kristine-
dc.contributor.authorVakhrusheva, Olesya-
dc.contributor.authorSlade, Kimberly Sue-
dc.contributor.authorThomas, Anita-
dc.contributor.authorTsaur, Igor-
dc.contributor.authorCinatl, Jindrich-
dc.contributor.authorMichaelis, Martin-
dc.contributor.authorEfferth, Thomas-
dc.contributor.authorHaferkamp, Axel-
dc.contributor.authorJuengel, Eva-
dc.date.accessioned2021-05-31T09:49:25Z-
dc.date.available2021-05-31T09:49:25Z-
dc.date.issued2021-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/5937-
dc.description.abstractThe prognosis for advanced prostate carcinoma (PCa) remains poor due to development of therapy resistance, and new treatment options are needed. Shikonin (SHI) from Traditional Chinese Medicine has induced antitumor effects in diverse tumor entities, but data related to PCa are scarce. Therefore, the parental (=sensitive) and docetaxel (DX)-resistant PCa cell lines, PC3, DU145, LNCaP, and 22Rv1 were exposed to SHI [0.1–1.5 μM], and tumor cell growth, proliferation, cell cycling, cell death (apoptosis, necrosis, and necroptosis), and metabolic activity were evaluated. Correspondingly, the expression of regulating proteins was assessed. Exposure to SHI time- and dose-dependently inhibited tumor cell growth and proliferation in parental and DX-resistant PCa cells, accompanied by cell cycle arrest in the G2/M or S phase and modulation of cell cycle regulating proteins. SHI induced apoptosis and more dominantly necroptosis in both parental and DX-resistant PCa cells. This was shown by enhanced pRIP1 and pRIP3 expression and returned growth if applying the necroptosis inhibitor necrostatin-1. No SHI-induced alteration in metabolic activity of the PCa cells was detected. The significant antitumor effects induced by SHI to parental and DX-resistant PCa cells make the addition of SHI to standard therapy a promising treatment strategy for patients with advanced PCa.en_GB
dc.description.sponsorshipOpen Access-Publizieren Universität Mainz / Universitätsmedizin Mainzde
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.titleShikonin reduces growth of docetaxel-resistant prostate cancer cells mainly through necroptosisen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-5928-
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.titleCancersde
jgu.journal.volume13de
jgu.journal.issue4de
jgu.pages.alternative882de
jgu.publisher.year2021-
jgu.publisher.nameMDPIde
jgu.publisher.placeBaselde
jgu.publisher.urihttps://doi.org/10.3390/cancers13040882de
jgu.publisher.issn2072-6694de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
jgu.publisher.doi10.3390/cancers13040882
jgu.organisation.rorhttps://ror.org/023b0x485
Appears in collections:JGU-Publikationen

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