Corrigendum to 'Sulforaphane Increases Drug-mediated Cytotoxicity Toward Cancer Stem-like Cells of Pancreas and Prostate'
| Autor: | Georgios Kallifatidis, Jury Gladkich, Juergen Mattern, Markus W. Büchler, Alexei V. Salnikov, Gerhard Moldenhauer, Vanessa Rausch, Ingrid Herr, Sabrina Labsch |
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| Jazyk: | angličtina |
| Rok vydání: | 2011 |
| Předmět: |
Male
Apoptosis Antioxidants chemistry.chemical_compound Mice Prostate Isothiocyanates Drug Discovery Antineoplastic Combined Chemotherapy Protocols Receptor Notch1 Cytotoxicity Tumor Stem Cell Assay media_common Mice Inbred BALB C Drug Synergism Molecular therapy Isoenzymes medicine.anatomical_structure Sulfoxides Neoplastic Stem Cells Molecular Medicine Female Pancreas Corrigendum Drug media_common.quotation_subject Mice Nude Aldehyde Dehydrogenase 1 Family Cell Line Tumor Spheroids Cellular Genetics medicine Animals Molecular Biology Pharmacology business.industry Cancer Prostatic Neoplasms Retinal Dehydrogenase Aldehyde Dehydrogenase medicine.disease Proto-Oncogene Proteins c-rel Pancreatic Neoplasms chemistry Cancer research business Thiocyanates Sulforaphane |
| Popis: | Despite intense efforts to develop treatments against pancreatic cancer, agents that cure this highly resistant and metastasizing disease are not available. Considerable attention has focused on broccoli compound sulforaphane (SF), which is suggested as combination therapy for targeting of pancreatic cancer stem cells (CSCs). However, there are concerns that antioxidative properties of SF may interfere with cytotoxic drugs-as suggested, e.g., for vitamins. Therefore we investigated a combination therapy using established pancreatic CSCs. Although cisplatin (CIS), gemcitabine (GEM), doxorubicin, 5-flurouracil, or SF effectively induced apoptosis and prevented viability, combination of a drug with SF increased toxicity. Similarly, SF potentiated the drug effect in established prostate CSCs revealing that SF enhances drug cytotoxicity also in other tumor entities. Most importantly, combined treatment intensified inhibition of clonogenicity and spheroid formation and aldehyde dehydrogenase 1 (ALDH1) activity along with Notch-1 and c-Rel expression indicating that CSC characteristics are targeted. In vivo, combination treatment was most effective and totally abolished growth of CSC xenografts and tumor-initiating potential. No pronounced side effects were observed in normal cells or mice. Our data suggest that SF increases the effectiveness of various cytotoxic drugs against CSCs without inducing additional toxicity in mice. |
| Databáze: | OpenAIRE |
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