Correlation of CD44 expression with proliferative activity of normal human breast epithelial cells in culture

Cooper, Nancy L.; Bardy, Peter; Bacani, Julinor; Kuusk, Urve; Dougherty, Graeme J.; Eaves, Connie J.; Emerman, Joanne T.

doi:10.1023/a:1006006425904

Cited by 10 publications

(4 citation statements)

References 23 publications

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“…6 and 7a). Increased CD44 has been reported previously in cultured mammary cells and was attributed to their increased rate of proliferation in culture 34 . Furthermore, CD44 is a Wnt target gene and may be induced by R-spondin 1 in the organoid culture medium 35 .…”

Section: Mammary Lineages Form Distinct Organoid Morphologiessupporting

confidence: 67%

Organoid cultures from normal and cancer-prone human breast tissues preserve complex epithelial lineages

et al. 2020

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Recently, organoid technology has been used to generate a large repository of breast cancer organoids. Here we present an extensive evaluation of the ability of organoid culture technology to preserve complex stem/progenitor and differentiated cell types via long-term propagation of normal human mammary tissues. Basal/stem and luminal progenitor cells can differentiate in culture to generate mature basal and luminal cell types, including ER+ cells that have been challenging to maintain in culture. Cells associated with increased cancer risk can also be propagated. Single-cell analyses of matched organoid cultures and native tissues by mass cytometry for 38 markers provide a higher resolution representation of the multiple mammary epithelial cell types in the organoids, and demonstrate that protein expression patterns of the tissue of origin can be preserved in culture. These studies indicate that organoid cultures provide a valuable platform for studies of mammary differentiation, transformation, and breast cancer risk.

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Section: Mammary Lineages Form Distinct Organoid Morphologiessupporting

confidence: 67%

Organoid cultures from normal and cancer-prone human breast tissues preserve complex epithelial lineages

et al. 2020

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“…The role of CD44v6 in these benign ductal cells is not known. Cooper et al 21 . have suggested that CD44v6 might be expressed occasionally in normal human breast epithelial cells as a response to cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

Expression of CD44s, CD44v3 and CD44v6 in benign and malignant breast lesions: correlation and colocalization with hyaluronan

Auvinen

Tammi²,

Tammi³

et al. 2005

Histopathology

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“…High expression of CD44 was found during in vitro repair of bronchial epithelial cells after a mechanical injury (31). CD44 can also stimulate cell proliferation (14), and CD44 upregulation has been demonstrated in areas of damaged bronchial epithelium both in normal and asthmatic subjects, strongly suggesting that CD44 may be directly or indirectly associated with repair processes occurring after damage (27). As for integrins, a new concept is emerging to suggest that integrins are multifunctional and may contribute not only to epithelial cell adhesion but also to regulation of cell growth and proliferation via a signaling pathway involving mitogen-activated protein kinase (18).…”

Section: Dep Exposure Is Associated With a Reduction Of The Hbe Cell mentioning

confidence: 99%

Negative impact of DEP exposure on human airway epithelial cell adhesion, stiffness, and repair

Doornaert

Leblond

Galiacy

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

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Epidemiological and experimental studies suggest that diesel exhaust particles (DEPs) may be associated with increased respiratory mortality and morbidity. Several recent studies have also shown that DEPs increase the production of inflammatory cytokines by human bronchial epithelium (HBE) cells in vitro. The present study investigates the effects of DEPs on the interaction of l-HBE cells (16HBE14o-) with the cell and matrix microenvironment based on evaluation of integrin-type cell/ matrix ligand expression, cytoskeleton (CSK) stiffness, and matrix remodeling via matrix metalloproteinase (MMP)-1, MMP-2, and MMP-9 expression. The results showed that DEP exposure induced: 1) a net dose-dependent decrease in CSK stiffness through actin fibers, 2) a concomitant specific reduction of both ␣ 3-and ␤1-integrin subunits extensively expressed on the HBE cell surface, 3) a decrease in the level of CD44, which is a major HBE cell-cell and HBE cell-matrix adhesion molecule; and 4) an isolated decrease in MMP-1 expression without any change in tissue inhibitor of matrix metalloproteinase (TIMP)-1 or TIMP-2 tissue inhibitors. Restrictive modulation of cell-matrix interaction, cell-cell connection, CSK stiffness, and fibrillary collagen remodeling results in a decreased wound closure capacity and an increased deadhesion capacity. In conclusion, on the basis of these results, we can propose that, in addition to their ability to increase the production of inflammatory cytokines, DEPs could also alter the links between actin CSK and the extracellular matrix, suggesting that they might facilitate HBE cell detachment in vivo. Airway epithelial cells are the primary target for air pollution and may play a key role in the pathophysiology of airway diseases. Recent studies have emphasized the role of DEPs in the development of an inflammatory response of bronchial epithelial cells. In vitro studies have shown that exposure of human bronchial epithelial (HBE) cells to DEPs significantly increased cell electrical resistance, decreased ciliary beat frequency (4), and induced release of interleukin (IL)-1␤, IL-8, and granulocyte-macrophage colony-stimulating factor (GM-CSF) inflammatory cytokines (4, 6, 7). However, although the proinflammatory impact of DEPs on bronchial epithelium is starting to be elucidated, little or no information about the other possible biological effects of DEPs is available at the present time. In particular, bronchial epithelial cells establish intercellular tight junctions and adhere to underlying basement membranes, which in turn may regulate bronchial epithelial cell shape, cell proliferation, and differentiation. In pulmonary diseases such as asthma, damage to bronchial epithelium is often associated with disruption of the underlying basement membrane and cell-cell interactions (34). On the basis of these data, it appeared important to determine whether DEPs may impair the interaction of bronchial epithelial cells with the matrix and cellular microenvironment.

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Correlation of CD44 expression with proliferative activity of normal human breast epithelial cells in culture

Cited by 10 publications

References 23 publications

Organoid cultures from normal and cancer-prone human breast tissues preserve complex epithelial lineages

Organoid cultures from normal and cancer-prone human breast tissues preserve complex epithelial lineages

Expression of CD44s, CD44v3 and CD44v6 in benign and malignant breast lesions: correlation and colocalization with hyaluronan

Negative impact of DEP exposure on human airway epithelial cell adhesion, stiffness, and repair

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