Abstract
Although human cancers exhibit intratumour heterogeneity, the influence of the tumour environment on this property is unclear. Single basal-like mammary epithelial cells are now shown to engage a dynamic TGFBR3-JUND signalling circuit in an extracellular-matrix-dependent manner. Cell transition between the distinct gene expression states underlying this circuit alters their properties and may modulate their propensity to malignancy.
MeSH terms
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Animals
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Breast Neoplasms / metabolism*
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Carcinoma, Intraductal, Noninfiltrating / metabolism*
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Female
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Humans
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Keratin-5 / metabolism*
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Proteoglycans / metabolism*
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Proto-Oncogene Proteins c-jun / metabolism*
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Receptors, Transforming Growth Factor beta / metabolism*
Substances
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JunD protein, human
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KRT5 protein, human
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Keratin-5
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Proteoglycans
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Proto-Oncogene Proteins c-jun
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Receptors, Transforming Growth Factor beta
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betaglycan