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• W2051218702 abstract "Cancer stem cells (CSCs) are a promising target for treating cancer, yet how CSC plasticity is maintained in vivo is unclear and is difficult to study in vitro. Here we establish a sustainable primary culture of Oct3/4(+)/Nanog(+) lung CSCs fed with CD90(+) cancer-associated fibroblasts (CAFs) to further advance our knowledge of preserving stem cells in the tumour microenvironment. Using transcriptomics we identify the paracrine network by which CAFs enrich CSCs through de-differentiation and reacquisition of stem cell-like properties. Specifically, we find that IGF1R signalling activation in cancer cells in the presence of CAFs expressing IGF-II can induce Nanog expression and promote stemness. Moreover, this paracrine signalling predicts overall and relapse-free survival in stage I non-small cell lung cancer (NSCLC) patients. IGF-II/IGF1R signalling blockade inhibits Nanog expression and attenuates cancer stem cell features. Our data demonstrate that CAFs constitute a supporting niche for cancer stemness, and targeting this paracrine signalling may present a new therapeutic strategy for NSCLC. Cancer stem cells are a sub-population of tumour cells but how they interact with the tumour microenvironment is unclear. Here, Chen et al.culture lung cancer stem cells with cancer-associated fibroblasts and delineate a signalling pathway between the two cells that helps maintain the cancer stem cell state." @default.
• W2051218702 created "2016-06-24" @default.
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• W2051218702 date "2014-03-25" @default.
• W2051218702 modified "2023-10-18" @default.
• W2051218702 title "Cancer-associated fibroblasts regulate the plasticity of lung cancer stemness via paracrine signalling" @default.
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• W2051218702 doi "https://doi.org/10.1038/ncomms4472" @default.
• W2051218702 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24668028" @default.
• W2051218702 hasPublicationYear "2014" @default.
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