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SOX11 promotes invasive growth and ductal carcinoma in situ progression.

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Publication Date
2017-10
ICR Author
Howard, Beatrice
Daley, Frances
Haider, Syed
Tomita, Naoko
Oliemuller Garcia, Erik
Author
Oliemuller, E
Kogata, N
Bland, P
Kriplani, D
Daley, F
Haider, S
Shah, V
Sawyer, EJ
Howard, BA
Type
Journal Article
Metadata
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Abstract
Here, we show that SOX11, an embryonic mammary marker that is normally silent in postnatal breast cells, is expressed in many oestrogen receptor-negative preinvasive ductal carcinoma in situ (DCIS) lesions. Mature mammary epithelial cells engineered to express SOX11 showed alterations in progenitor cell populations, including an expanded basal-like population with increased aldehyde dehydrogenase (ALDH) activity, and increased mammosphere-forming capacity. DCIS.com cells engineered to express SOX11 showed increased ALDH activity, which is a feature of cancer stem cells. The CD44+/CD24-/ALDH+ cell population was increased in DCIS.com cells that expressed SOX11. Upregulating SOX11 expression in DCIS.com cells led to increased invasive growth both in vitro and when they were injected intraductally in a mouse model of DCIS that recapitulates human disease. Invasive lesions formed sooner and tumour growth was augmented in vivo, suggesting that SOX11 contributes to the progression of DCIS to invasive breast cancer. We identified potential downstream effectors of SOX11 during both microinvasive and invasive tumour growth stages, including several with established links to regulation of progenitor cell function and prenatal developmental growth. Our findings suggest that SOX11 is a potential biomarker for DCIS lesions containing cells harbouring distinct biological features that are likely to progress to invasive breast cancer. © 2017 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.
URL
https://repository.icr.ac.uk/handle/internal/697
Collections
  • Breast Cancer Research
Licenseref URL
https://creativecommons.org/licenses/by/4.0
Version of record
10.1002/path.4939
Subject
Mammary Glands, Animal
Epithelial Cells
Stem Cells
Animals
Humans
Mice, SCID
Carcinoma, Ductal, Breast
Breast Neoplasms
Disease Progression
Aldehyde Dehydrogenase
Up-Regulation
Female
SOXC Transcription Factors
Research team
Endocrine control mechanisms
Molecular Cell Biology
Language
eng
Date accepted
2017-06-23
License start date
2017-10
Citation
The Journal of pathology, 2017, 243 (2), pp. 193 - 207

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