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Phenotypic heterogeneity of disseminated tumour cells is preset by primary tumour hypoxic microenvironments
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Phenotypic heterogeneity of disseminated tumour cells is preset by primary tumour hypoxic microenvironments
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Journal Article
Phenotypic heterogeneity of disseminated tumour cells is preset by primary tumour hypoxic microenvironments
2017
Overview
Hypoxia is a poor-prognosis microenvironmental hallmark of solid tumours, but it is unclear how it influences the fate of disseminated tumour cells (DTCs) in target organs. Here we report that hypoxic HNSCC and breast primary tumour microenvironments displayed upregulation of key dormancy (NR2F1, DEC2, p27) and hypoxia (GLUT1, HIF1α) genes. Analysis of solitary DTCs in PDX and transgenic mice revealed that post-hypoxic DTCs were frequently NR2F1
hi
/DEC2
hi
/p27
hi
/TGFβ2
hi
and dormant. NR2F1 and HIF1α were required for p27 induction in post-hypoxic dormant DTCs, but these DTCs did not display GLUT1
hi
expression. Post-hypoxic DTCs evaded chemotherapy and, unlike ER
−
breast cancer cells, post-hypoxic ER
+
breast cancer cells were more prone to enter NR2F1-dependent dormancy. We propose that primary tumour hypoxic microenvironments give rise to a subpopulation of dormant DTCs that evade therapy. These post-hypoxic dormant DTCs may be the source of disease relapse and poor prognosis associated with hypoxia.
Aguirre-Ghiso and colleagues report that hypoxia in the primary tumour microenvironment leads to upregulation of a dormancy signature in the tumour cells that persists after their dissemination to distant sites, permitting them to evade therapy.
Publisher
Nature Publishing Group UK,Nature Publishing Group
