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• W2216993934 abstract "Development of resistance represents a major drawback in osteosarcoma treatment, despite improvements in overall survival. Treatment failure and tumor progression have been attributed to pre-existing drug-resistant clones commonly assigned to a cancer stem-like phenotype. Evidence suggests that non stem-like cells, when submitted to certain microenvironmental stimuli, can acquire a stemness phenotype thereby strengthening their capacity to handle with stressful conditions. Here, using osteosarcoma cell lines and a mouse xenograft model, we show that exposure to conventional chemotherapeutics induces a phenotypic cell transition toward a stem-like phenotype. This associates with activation of Wnt/β-catenin signaling, up-regulation of pluripotency factors and detoxification systems (ABC transporters and Aldefluor activity) that ultimately leads to chemotherapy failure. Wnt/β-catenin inhibition combined with doxorubicin, in the MNNG-HOS cells, prevented the up-regulation of factors linked to transition into a stem-like state and can be envisaged as a way to overcome adaptive resistance. Finally, the analysis of the public R2 database, containing microarray data information from diverse osteosarcoma tissues, revealed a correlation between expression of stemness markers and a worse response to chemotherapy, which provides evidence for drug-induced phenotypic stem cell state transitions in osteosarcoma." @default.
• W2216993934 created "2016-06-24" @default.
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• W2216993934 date "2016-01-01" @default.
• W2216993934 modified "2023-10-13" @default.
• W2216993934 title "Chemotherapy induces stemness in osteosarcoma cells through activation of Wnt/β-catenin signaling" @default.
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• W2216993934 doi "https://doi.org/10.1016/j.canlet.2015.11.013" @default.
• W2216993934 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26577806" @default.
• W2216993934 hasPublicationYear "2016" @default.
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