CD44 Modulates Hs578T Human Breast Cancer Cell Adhesion, Migration, and Invasiveness

Herrera-Gayol, Andrea; Jothy, Serge

doi:10.1006/exmp.1999.2236

Cited by 52 publications

(31 citation statements)

References 43 publications

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“…By binding to fibronectin and vitronectin, tumor cells can invade the extracellular matrix [39,40]. Herrera-Gayol and Jothy [41] suggested that CD44 (especially CDv6) on breast cancer cells regulates binding to extracellular HA and is involved in metastasis. Since most integrins bind to the extracellular matrix, most studies on metastasis have focused on this interaction.…”

Section: Discussionmentioning

confidence: 99%

CD44 Cross-linking induces integrin-mediated adhesion and transendothelial migration in breast cancer cell line by up-regulation of LFA-1 (αLβ2) and VLA-4 (α4β1)

Wang¹,

Hung²,

et al. 2005

Experimental Cell Research

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Section: Discussionmentioning

confidence: 99%

CD44 Cross-linking induces integrin-mediated adhesion and transendothelial migration in breast cancer cell line by up-regulation of LFA-1 (αLβ2) and VLA-4 (α4β1)

Wang¹,

Hung²,

et al. 2005

Experimental Cell Research

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“…Functional studies have demonstrated an important role of the expression of CD44 variants and metastasis (Gunther et al, 1991;Herrera-Gayol and Jothy, 1999). These observations led us to question whether and how regulation of the expression of CD44 isoforms, including the commonly expressed CD44v6 variant, would affect the metastatic ability of HM7 colon cancer cells.…”

Section: Discussionmentioning

confidence: 99%

“…Homotypic and heterotypic, cell-to-cell and cell-to-matrix interactions are involved in each of these steps (Herrera-Gayol and Jothy, 1999). CD44 is one of the few proteins able to fulfil this dual role.…”

mentioning

confidence: 99%

Butyrate down-regulates CD44 transcription and liver colonisation in a highly metastatic human colon carcinoma cell line

et al. 2002

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Over-expression of the adhesion molecule CD44 and its splice variants, especially CD44v6, is associated with poor prognosis and metastasis. We aimed at regulating the expression of CD44 in the highly metastatic human colon cancer cell line HM7 and thereby affecting its metastatic ability. HM7 cells show constitutive expression of CD44 standard and variants isoforms, which were significantly down-regulated by treatment with butyrate. Butyrate significantly inhibited transcription of the CD44 gene and abolished epidermal growth factor-mediated up-regulation of the reporter gene luciferase subcloned upstream to the CD44 promoter ( -1.1 kb) and transfected to HM7 cells. Nuclear proteins from butyrate-treated cells bound to an epidermal growth factor receptor element motif present in the CD44 promoter. Epidermal growth factor receptor elementsite directed mutations eliminated the inducibility of the luciferase reporter gene and did not allowed binding of nuclear proteins harvested from butyrate-treated cells. Butyrate induced CD44 gene repression by specifically interacting with an epidermal growth factor receptor element nuclear transcriptional factor. This interaction affects CD44 transcriptional activity vis-à-vis in vivo metastatic ability of HM7 cells. These results provide additional insight into the anticarcinogenic properties of butyrate.

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“…Alternative splicing along with post-translational modifications have rendered CD44 a protein with diverse functions. Although CD44 is linked to pathologic conditions, such as atherosclerosis (Cuff et al, 2001) and cancer metastasis (Herrera-Gayol and Jothy, 1999;Bourguignon et al, 2001;Wong et al, 2003), it also orchestrates many physiological processes such as cellcell and cell-matrix anchorage (Lazaar et al, 1994), extracellular matrix protein recycling (Kaya et al, 1999;Teder et al, 2002), angiogenesis (van Royen et al, 2004), inflammation (Teder et al, 2002), and T lymphocyte activation (Seth et al, 1991;Galandrini et al, 1994) in many cases through its interaction with HA. One of the major functions of CD44 appears to be the regulation of cell motility and chemotaxis (Katagiri et al, 1999;Fanning et al, 2005).…”

mentioning

confidence: 97%

CD44 regulates myoblast migration and differentiation

Mylona

Jones

Mills

et al. 2006

Journal Cellular Physiology

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CD44 is a transmembrane protein that plays a role in cell-cell interactions and motility in a number of cell types. Cell-cell interactions are critical for myoblast differentiation and fusion but whether CD44 regulates myogenesis is unknown. Here, we show that CD44 plays a functional role in early myogenesis. Analyses of myofiber cross-sectional area, after local injury in mouse tibialis anterior (TA) muscles, revealed that growth was transiently delayed in the absence of CD44. A muscle-intrinsic role for CD44 is suggested as primary myoblasts from CD44(-/-) mice displayed attenuated differentiation and subsequent myotube formation at early times in a differentiation-inducing in vitro environment. Chemotaxis of CD44(-/-) myoblasts toward hepatocyte growth factor (HGF) and basic fibroblast growth factor (bFGF) was totally abrogated, although expression of their respective receptors did not appear to differ from wild-type. Furthermore, motility of CD44(-/-) myoblasts was decreased at early stages of differentiation as determined by time-lapse microscopy. Wild-type myoblasts contained two subpopulations of slow- and fast-migrating cells, whereas CD44(-/-) myoblasts were composed predominantly of the slower migrating subpopulation. Taken together, these data suggest that myoblast migration and differentiation are closely linked and CD44 is a key regulator.

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CD44 Modulates Hs578T Human Breast Cancer Cell Adhesion, Migration, and Invasiveness

Cited by 52 publications

References 43 publications

CD44 Cross-linking induces integrin-mediated adhesion and transendothelial migration in breast cancer cell line by up-regulation of LFA-1 (αLβ2) and VLA-4 (α4β1)

CD44 Cross-linking induces integrin-mediated adhesion and transendothelial migration in breast cancer cell line by up-regulation of LFA-1 (αLβ2) and VLA-4 (α4β1)

Butyrate down-regulates CD44 transcription and liver colonisation in a highly metastatic human colon carcinoma cell line

CD44 regulates myoblast migration and differentiation

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