We are analyzing https://link.springer.com/article/10.1186/bcr3663.

Title:
Aldehyde dehydrogenase and estrogen receptor define a hierarchy of cellular differentiation in the normal human mammary epithelium | Breast Cancer Research
Description:
Introduction Although estrogen and progesterone play a key role in normal mammary development and in breast cancer, the potential for proliferation and lineage differentiation as well as origin of cells that express the estrogen receptor (ER) in normal breast epithelium are not known. Some evidence suggests that normal human mammary stem/progenitor cells are ER–, but the identity of these cells and the cellular hierarchy of breast epithelium are still subjects of controversy. It is likely that elucidation of these aspects will bring insight into the cellular origin of breast cancer subtypes. Methods We used fluorescence-activated cell sorting of primary human mammary epithelial cells along with in vitro and in vivo functional assays to examine the hierarchic relation between cells with aldehyde dehydrogenase enzymatic activity (ALDH+ cells) and ER+ cells in the normal human breast epithelium. We assessed the proliferation and lineage differentiation potential of these cells in vitro and in vivo. A gene reporter assay was used to separate live ER+ and ER– mammary epithelial cells. With shRNA-mediated knockdown, we investigated the role of ALDH isoforms in the functionality of mammary epithelial progenitor cells. Results We describe a cellular hierarchy in the normal human mammary gland in which ER–/ALDH+ cells with functional properties of stem/progenitor cells generate ER+ progenitor cells, which in turn give rise to cells of luminal lineage. We show that the ALDH1A1 isoform, through its function in the retinoic acid metabolism, affects the proliferation and/or early differentiation of stem/progenitor cells and is important for branching morphogenesis. Conclusions This study presents direct evidence that ER+ cells are generated by ER–/ALDH+ stem/progenitor cells. We also show that ER+ cells are able to generate cell progeny of luminal lineage in vitro and in vivo. Loss of ALDH1A1 function impairs this process, as well as branching morphogenesis and clonogenicity in suspension culture. This latter effect is reversed by treatment with retinoic acid.
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Keywords {🔍}

cells, aldha, mammary, cell, breast, pubmed, cancer, article, normal, epithelial, google, scholar, human, cas, figure, stem, aldh, stemprogenitor, expression, luminal, epithelium, additional, file, alde, generate, estrogen, culture, population, vivo, receptor, proliferation, retinoic, acid, primary, generated, central, mammospheres, differentiation, sections, lineage, activity, isoforms, markers, gland, samples, research, progesterone, vitro, branching, tissue,

Topics {✒️}

er–/aldh+ stem/progenitor cells stem cell-related markers retinoic acid receptor-alpha cd49f-high/epcam-/lin mammary stem/progenitor cells stem/progenitor cell population normal stem/progenitor cells stem/progenitor cells identified article download pdf alde+ stem/progenitor cells progestin-regulated luminal cell luminal cell-fate commitment myoepithelial cell-specific responses unseparated live-cell populations biomedical research centre identify stem/progenitor cells pinder & gabriela dontu estrogen receptor-negative estrogen receptor alpha specific dna-binding sites gfp-sorted cells transduced author information authors christophe ginestier conjugated donkey anti-mouse routine tissue-processing procedures breakthrough breast cancer serum-free f12 media asselin-labat ml ultra-low attachment plates ultra-low-attachment plates short-range signals initiated cell stem cell full size image basal tumor development fluorescence-activated cell sorting human mammary gland human mammary epithelium flow-activated cell sorting estrogen receptor define brca1 healthy carriers human breast cancer epithelial progesterone receptor mammary epithelial cells human mammary fibroblasts estrogen receptor expression mammary stem cells lentivirus-mediated shrna interference broadest lineage-differentiation potential fat-pad section stained tukey multiple-comparisons test

Questions {❓}

Alison MR, Guppy NJ, Lim SM, Nicholson LJ: Finding cancer stem cells: are aldehyde dehydrogenases fit for purpose?

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         description:Although estrogen and progesterone play a key role in normal mammary development and in breast cancer, the potential for proliferation and lineage differentiation as well as origin of cells that express the estrogen receptor (ER) in normal breast epithelium are not known. Some evidence suggests that normal human mammary stem/progenitor cells are ER–, but the identity of these cells and the cellular hierarchy of breast epithelium are still subjects of controversy. It is likely that elucidation of these aspects will bring insight into the cellular origin of breast cancer subtypes. We used fluorescence-activated cell sorting of primary human mammary epithelial cells along with in vitro and in vivo functional assays to examine the hierarchic relation between cells with aldehyde dehydrogenase enzymatic activity (ALDH+ cells) and ER+ cells in the normal human breast epithelium. We assessed the proliferation and lineage differentiation potential of these cells in vitro and in vivo. A gene reporter assay was used to separate live ER+ and ER– mammary epithelial cells. With shRNA-mediated knockdown, we investigated the role of ALDH isoforms in the functionality of mammary epithelial progenitor cells. We describe a cellular hierarchy in the normal human mammary gland in which ER–/ALDH+ cells with functional properties of stem/progenitor cells generate ER+ progenitor cells, which in turn give rise to cells of luminal lineage. We show that the ALDH1A1 isoform, through its function in the retinoic acid metabolism, affects the proliferation and/or early differentiation of stem/progenitor cells and is important for branching morphogenesis. This study presents direct evidence that ER+ cells are generated by ER–/ALDH+ stem/progenitor cells. We also show that ER+ cells are able to generate cell progeny of luminal lineage in vitro and in vivo. Loss of ALDH1A1 function impairs this process, as well as branching morphogenesis and clonogenicity in suspension culture. This latter effect is reversed by treatment with retinoic acid.
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            Surgical Oncology
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               type:PostalAddress
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      name:Anand D Purushotham
      affiliation:
            name:King’s College London School of Medicine
            address:
               name:Research Oncology, King’s College London School of Medicine, London, UK
               type:PostalAddress
            type:Organization
      name:Sarah E Pinder
      affiliation:
            name:King’s College London School of Medicine
            address:
               name:Research Oncology, King’s College London School of Medicine, London, UK
               type:PostalAddress
            type:Organization
      name:Gabriela Dontu
      affiliation:
            name:King’s College London School of Medicine
            address:
               name:Stem Cell Group, Research Oncology, King’s College London School of Medicine, London, UK
               type:PostalAddress
            type:Organization
            name:King’s College London School of Medicine
            address:
               name:Research Oncology, King’s College London School of Medicine, London, UK
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Stem Cell Group, Research Oncology, King’s College London School of Medicine, London, UK
      name:Stem Cell Group, Research Oncology, King’s College London School of Medicine, London, UK
      name:Centre de Recherche en Cancérologie de Marseille, Laboratoire d’Oncologie Moléculaire, Inserm, CRCM, U1068, Marseille, France
      name:Department of Internal Medicine, University of Michigan, Ann Arbor, USA
      name:Department of Internal Medicine, University of Michigan, Ann Arbor, USA
      name:Department of Surgery, Cheil General Hospital & Women’s Healthcare Center, Kwandong University College of Medicine, Seoul, South Korea
      name:Stem Cell Group, Research Oncology, King’s College London School of Medicine, London, UK
      name:Breakthrough Breast Cancer Research Unit, King’s College London School of Medicine, London, UK
      name:Stem Cell Group, Research Oncology, King’s College London School of Medicine, London, UK
      name:Breakthrough Breast Cancer Research Unit, King’s College London School of Medicine, London, UK
      name:Stem Cell Group, Research Oncology, King’s College London School of Medicine, London, UK
      name:Breakthrough Breast Cancer Research Unit, King’s College London School of Medicine, London, UK
      name:Stem Cell Group, Research Oncology, King’s College London School of Medicine, London, UK
      name:Department of Health Sciences, University of Milano-Bicocca, Monza, Italy
      name:Research Oncology, King’s College London School of Medicine, London, UK
      name:Research Oncology, King’s College London School of Medicine, London, UK
      name:Research Oncology, King’s College London School of Medicine, London, UK
      name:Stem Cell Group, Research Oncology, King’s College London School of Medicine, London, UK
      name:Research Oncology, King’s College London School of Medicine, London, UK

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