Jagged1-Notch1-deployed tumor perivascular niche promotes breast cancer stem cell phenotype through Zeb1.

Abstract:

:Zinc finger E-box binding homeobox 1 (Zeb1) has been demonstrated to participate in the acquisition of the properties of cancer stem cells (CSCs). However, it is largely unknown how signals from the tumor microenvironment (TME) contribute to aberrant Zeb1 expression. Here, we show that Zeb1 depletion suppresses stemness, colonization and the phenotypic plasticity of breast cancer. Moreover, we demonstrate that, with direct cell-cell contact, TME-derived endothelial cells provide the Notch ligand Jagged1 (Jag1) to neighboring breast CSCs, leading to Notch1-dependent upregulation of Zeb1. In turn, ectopic Zeb1 in tumor cells increases VEGFA production and reciprocally induces endothelial Jag1 in a paracrine manner. Depletion of Zeb1 disrupts this positive feedback loop in the tumor perivascular niche, which eventually lessens tumor initiation and progression in vivo and in vitro. In this work, we highlight that targeting the angiocrine Jag1-Notch1-Zeb1-VEGFA loop decreases breast cancer aggressiveness and thus enhances the efficacy of antiangiogenic therapy.

journal_name

Nat Commun

journal_title

Nature communications

authors

Jiang H,Zhou C,Zhang Z,Wang Q,Wei H,Shi W,Li J,Wang Z,Ou Y,Wang W,Wang H,Zhang Q,Sun W,Sun P,Yang S

doi

10.1038/s41467-020-18860-4

subject

Has Abstract

pub_date

2020-10-12 00:00:00

pages

5129

issue

1

issn

2041-1723

pii

10.1038/s41467-020-18860-4

journal_volume

11

pub_type

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