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dc.contributor.authorÖzenver, Nadire
dc.contributor.authorSaeed, Mohamed
dc.contributor.authorDemirezer, Lütfiye Ömur
dc.contributor.authorEfferth, Thomas
dc.date.accessioned2019-12-16T10:09:21Z
dc.date.available2019-12-16T10:09:21Z
dc.date.issued2018
dc.identifier.issn1949-2553
dc.identifier.urihttps://doi.org/10.18632/oncotarget.24880
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5915154/
dc.identifier.urihttp://hdl.handle.net/11655/19890
dc.description.abstractAs a leading cause of global mortality, cancer frequently cannot be cured due to the development of drug resistance. Therefore, novel drugs are required. Naturally occurring anthraquinones are mostly present in Rumex and Rhamnus species and are of interest because of their structural similarity to anthracyclines as well established anticancer drugs. In the present study, we focused on the structural elucidation of phytochemicals from R. acetosella as well as the investigation of cytotoxicity and modes of action of the main anthraquinone aglycons (emodin, Aloe-emodin, physcion, rhein). Resazurin reduction and protease viability marker assays were conducted to test their cytotoxicity. Microarray-based gene expression profiling was performed to identify cellular pathways affected by the compounds, which was validated by qPCR analyses and functional assays. Flow cytometry was used to measure cell cycle distribution, apoptosis and necrosis, induction of reactive oxygen species (ROS) and disruption of mitochondrial membrane potential (MMP). The comet assay was used to detect DNA damage. Aloe-emodin as the most cytotoxic compound revealed IC50 values from 9.872 μM to 22.3 μM in drug-sensitive wild-type cell lines and from 11.19 μM to 33.76 μM in drug-resistant sublines, was selected to investigate its mechanism against cancer. Aloe-emodin-induced S phase arrest, ROS generation, DNA damage and apoptosis. Microarray hybridization revealed a profile of deregulated genes in Aloe-emodin-treated CCRF-CEM cells with diverse functions such as cell death and survival, cellular growth and proliferation, cellular development, gene expression, cellular function and maintenance. Aloe-emodin as well as R. acetosella deserve further investigations as possible antineoplastic drug candidates.
dc.relation.isversionof10.18632/oncotarget.24880
dc.rightsinfo:eu-repo/semantics/openAccess
dc.titleAloe-Emodin As Drug Candidate For Cancer Therapy
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:eu-repo/semantics/publishedVersion
dc.relation.journalOncotarget
dc.contributor.departmentFarmakognozi
dc.identifier.volume9
dc.identifier.issue25
dc.identifier.startpage17770
dc.identifier.endpage17796
dc.description.indexPubMed
dc.description.indexScopus


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