ID4 controls mammary stem cells and marks breast cancers with a stem cell-like phenotype.

Junankar, S; Baker, LA; Roden, DL; Nair, R; Elsworth, B; Gallego-Ortega, D; Lacaze, P; Cazet, A; Nikolic, I; Teo, WS; Yang, J; McFarland, A; Harvey, K; Naylor, MJ; Lakhani, SR; Simpson, PT; Raghavendra, A; Saunus, J; Madore, J; Kaplan, W; Ormandy, C; Millar, EKA; O'Toole, S; Yun, K; Swarbrick, A

ID4 controls mammary stem cells and marks breast cancers with a stem cell-like phenotype.

Junankar, S Baker, LA Roden, DL Nair, R Elsworth, B Gallego-Ortega, D Lacaze, P Cazet, A Nikolic, I Teo, WS Yang, J McFarland, A Harvey, K Naylor, MJ Lakhani, SR Simpson, PT Raghavendra, A Saunus, J Madore, J Kaplan, W Ormandy, C Millar, EKA O'Toole, S Yun, K Swarbrick, A

Permalink

Publisher:: NATURE PUBLISHING GROUP
Publication Type:: Journal Article
Citation:: Nat Commun, 2015, 6, (1), pp. 6548
Issue Date:: 2015-03-27

Closed Access

	Filename	Description	Size
	ncomms7548.pdf		1.71 MB	Adobe PDF	View/Open

Copyright Clearance Process

Recently Added
In Progress
Closed Access

This item is closed access and not available.

Full metadata record

Field	Value	Language
dc.contributor.author	Junankar, S
dc.contributor.author	Baker, LA
dc.contributor.author	Roden, DL
dc.contributor.author	Nair, R
dc.contributor.author	Elsworth, B
dc.contributor.author	Gallego-Ortega, D
dc.contributor.author	Lacaze, P
dc.contributor.author	Cazet, A
dc.contributor.author	Nikolic, I
dc.contributor.author	Teo, WS
dc.contributor.author	Yang, J
dc.contributor.author	McFarland, A
dc.contributor.author	Harvey, K
dc.contributor.author	Naylor, MJ
dc.contributor.author	Lakhani, SR
dc.contributor.author	Simpson, PT
dc.contributor.author	Raghavendra, A
dc.contributor.author	Saunus, J
dc.contributor.author	Madore, J
dc.contributor.author	Kaplan, W
dc.contributor.author	Ormandy, C
dc.contributor.author	Millar, EKA
dc.contributor.author	O'Toole, S
dc.contributor.author	Yun, K
dc.contributor.author	Swarbrick, A
dc.date.accessioned	2022-04-13T12:47:23Z
dc.date.available	2015-02-04
dc.date.available	2022-04-13T12:47:23Z
dc.date.issued	2015-03-27
dc.identifier.citation	Nat Commun, 2015, 6, (1), pp. 6548
dc.identifier.issn	2041-1723
dc.identifier.issn	2041-1723
dc.identifier.uri	http://hdl.handle.net/10453/156229
dc.description.abstract	Basal-like breast cancer (BLBC) is a heterogeneous disease with poor prognosis; however, its cellular origins and aetiology are poorly understood. In this study, we show that inhibitor of differentiation 4 (ID4) is a key regulator of mammary stem cell self-renewal and marks a subset of BLBC with a putative mammary basal cell of origin. Using an ID4GFP knock-in reporter mouse and single-cell transcriptomics, we show that ID4 marks a stem cell-enriched subset of the mammary basal cell population. ID4 maintains the mammary stem cell pool by suppressing key factors required for luminal differentiation. Furthermore, ID4 is specifically expressed by a subset of human BLBC that possess a very poor prognosis and a transcriptional signature similar to a mammary stem cell. These studies identify ID4 as a mammary stem cell regulator, deconvolute the heterogeneity of BLBC and link a subset of mammary stem cells to the aetiology of BLBC.
dc.format	Electronic
dc.language	eng
dc.publisher	NATURE PUBLISHING GROUP
dc.relation.ispartof	Nat Commun
dc.relation.isbasedon	10.1038/ncomms7548
dc.rights	info:eu-repo/semantics/closedAccess
dc.subject.mesh	Animals
dc.subject.mesh	Breast Neoplasms
dc.subject.mesh	Cell Line, Tumor
dc.subject.mesh	Female
dc.subject.mesh	Gene Knock-In Techniques
dc.subject.mesh	Humans
dc.subject.mesh	Inhibitor of Differentiation Proteins
dc.subject.mesh	Mammary Glands, Animal
dc.subject.mesh	Mice
dc.subject.mesh	Neoplasm Transplantation
dc.subject.mesh	Phenotype
dc.subject.mesh	RNA, Messenger
dc.subject.mesh	Real-Time Polymerase Chain Reaction
dc.subject.mesh	Stem Cells
dc.subject.mesh	Mammary Glands, Animal
dc.subject.mesh	Cell Line, Tumor
dc.subject.mesh	Stem Cells
dc.subject.mesh	Animals
dc.subject.mesh	Humans
dc.subject.mesh	Mice
dc.subject.mesh	Breast Neoplasms
dc.subject.mesh	RNA, Messenger
dc.subject.mesh	Neoplasm Transplantation
dc.subject.mesh	Phenotype
dc.subject.mesh	Female
dc.subject.mesh	Inhibitor of Differentiation Proteins
dc.subject.mesh	Gene Knock-In Techniques
dc.subject.mesh	Real-Time Polymerase Chain Reaction
dc.title	ID4 controls mammary stem cells and marks breast cancers with a stem cell-like phenotype.
dc.type	Journal Article
utslib.citation.volume	6
utslib.location.activity	England
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Engineering and Information Technology
pubs.organisational-group	/University of Technology Sydney/Faculty of Engineering and Information Technology/School of Biomedical Engineering
pubs.organisational-group	/University of Technology Sydney/Centre for Health Technologies (CHT)
utslib.copyright.status	closed_access	*
dc.date.updated	2022-04-13T12:47:21Z
pubs.issue	1
pubs.publication-status	Published online
pubs.volume	6
utslib.citation.issue	1

Abstract:

Basal-like breast cancer (BLBC) is a heterogeneous disease with poor prognosis; however, its cellular origins and aetiology are poorly understood. In this study, we show that inhibitor of differentiation 4 (ID4) is a key regulator of mammary stem cell self-renewal and marks a subset of BLBC with a putative mammary basal cell of origin. Using an ID4GFP knock-in reporter mouse and single-cell transcriptomics, we show that ID4 marks a stem cell-enriched subset of the mammary basal cell population. ID4 maintains the mammary stem cell pool by suppressing key factors required for luminal differentiation. Furthermore, ID4 is specifically expressed by a subset of human BLBC that possess a very poor prognosis and a transcriptional signature similar to a mammary stem cell. These studies identify ID4 as a mammary stem cell regulator, deconvolute the heterogeneity of BLBC and link a subset of mammary stem cells to the aetiology of BLBC.

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/156229