A tumour promoter induces alterations in vinculin and actin distribution in human renal epithelium

Maeve A. Rahilly, Stewart Fleming

    Research output: Contribution to journalArticle

    11 Citations (Scopus)

    Abstract

    Loss of cell-substratum adhesion is an important factor during tumour progression. We have previously described reduced focal contact components and poorly organized cytoskeletal actin in renal cell carcinomas. In this study, we have used the potent tumour promoter TPA on cultured human renal epithelium to mimic neoplastic transformation. The morphological changes induced by TPA were examined by phase contrast and fluorescence microscopy. TPA treatment caused rounding up of cells and loss of adhesion to either fibronectin or laminin substrata. Cytoskeletal actin was redistributed from orientated stress fibre bundles to a perinuclear circumferential arrangement. This was accompanied by a progressive reduction in the number of vinculin-containing contacts with accumulation of vinculin in punctate spots in the perinuclear region. These altered membrane-cytoskeletal interactions induced by TPA are entirely reversible and mimic epigenetic changes which occur during tumour progression.
    Original languageEnglish
    Pages (from-to)283-8
    Number of pages6
    JournalJournal of Pathology
    Volume166
    Issue number3
    DOIs
    Publication statusPublished - Mar 1992

    Fingerprint

    Vinculin
    Cell Adhesion
    Carcinogens
    Actins
    Epithelium
    Kidney
    Phase-Contrast Microscopy
    Stress Fibers
    Focal Adhesions
    Laminin
    Fibronectins
    Fluorescence Microscopy
    Renal Cell Carcinoma
    Epigenomics
    Neoplasms
    Membranes

    Cite this

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    title = "A tumour promoter induces alterations in vinculin and actin distribution in human renal epithelium",
    abstract = "Loss of cell-substratum adhesion is an important factor during tumour progression. We have previously described reduced focal contact components and poorly organized cytoskeletal actin in renal cell carcinomas. In this study, we have used the potent tumour promoter TPA on cultured human renal epithelium to mimic neoplastic transformation. The morphological changes induced by TPA were examined by phase contrast and fluorescence microscopy. TPA treatment caused rounding up of cells and loss of adhesion to either fibronectin or laminin substrata. Cytoskeletal actin was redistributed from orientated stress fibre bundles to a perinuclear circumferential arrangement. This was accompanied by a progressive reduction in the number of vinculin-containing contacts with accumulation of vinculin in punctate spots in the perinuclear region. These altered membrane-cytoskeletal interactions induced by TPA are entirely reversible and mimic epigenetic changes which occur during tumour progression.",
    author = "Rahilly, {Maeve A.} and Stewart Fleming",
    year = "1992",
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    A tumour promoter induces alterations in vinculin and actin distribution in human renal epithelium. / Rahilly, Maeve A.; Fleming, Stewart.

    In: Journal of Pathology, Vol. 166, No. 3, 03.1992, p. 283-8.

    Research output: Contribution to journalArticle

    TY - JOUR

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    AU - Fleming, Stewart

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    AB - Loss of cell-substratum adhesion is an important factor during tumour progression. We have previously described reduced focal contact components and poorly organized cytoskeletal actin in renal cell carcinomas. In this study, we have used the potent tumour promoter TPA on cultured human renal epithelium to mimic neoplastic transformation. The morphological changes induced by TPA were examined by phase contrast and fluorescence microscopy. TPA treatment caused rounding up of cells and loss of adhesion to either fibronectin or laminin substrata. Cytoskeletal actin was redistributed from orientated stress fibre bundles to a perinuclear circumferential arrangement. This was accompanied by a progressive reduction in the number of vinculin-containing contacts with accumulation of vinculin in punctate spots in the perinuclear region. These altered membrane-cytoskeletal interactions induced by TPA are entirely reversible and mimic epigenetic changes which occur during tumour progression.

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