Surface sialic acid reduces attachment of metastatic tumour cells to collagen type IV and fibronectin

Dennis, Jim; Waller, C. A.; Timpl, Rupert; Schirrmacher, Volker

doi:10.1038/300274a0

Cited by 204 publications

(130 citation statements)

References 24 publications

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“…Between 15 and 25% of sialic acid was released by neuraminidase from both high and low metastatic cells, which is similar to some other high metastatic lines (Dennis et al, 1982;Yogeeswaran & Salk, 1981). The proportion of sialylated galactose and N-acetyl galactose was similar in 1G8 and 1G3.…”

Section: Aggregation and Disaggregation The Results Insupporting

confidence: 53%

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Morphological and metastatic murine melanoma variants: motility, adhesiveness, cell surface and in vivo properties

Clark¹,

Js²,

Sidebottom³

1987

Br J Cancer

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The results show enhanced differences in metastatic potential of tight and loose clones after selective cloning and that there may be important differences in motility and cell-substrate interactions. Foulds (1949) introduced the term tumour progression to describe the process by which some tumours become more malignant during their growth. Nowell (1976) attributed this to genetic instability, although genetic or epigenetic processes could result in the emergence of variant cells with growth advantages which differ from the main population in the expression of specific characters (Frost & Kerbel, 1983;Schimke et al., 1985).The existence within tumours of cells heterogeneous for the expression of a wide range of in vivo and in vitro characters is well documented (for reviews see Heppner, 1984;Nicolson, 1984).We have previously reported heterogeneity of clonal morphology in a metastatic melanomaxlymphocyte hybrid tumour cell line (Clark & Sidebottom, 1984). These variants grow either as tight or loose colonies and the isolation of cell lines, stable for clonal morphology, which have low or high metastatic phenotypes has been described (Clark & Sidebottom, 1984). The morphology and patterns of growth of these variants suggests a number of ways in which these cells may differ and which might account for their behavioural differences in vitro. These include intercellular and cell-substrate adhesion and motility, which in turn are dependent upon cell surface properties. Various stages of the metastatic cascade, for example local invasion or tumourcapillary endothelium adhesion are partially dependent upon intercellular and cell-substrate adhesion and motility (Weiss, 1980;Varani et al., 1980;Nicolson et al., 1986). The cell surface has an important role in these interactions and has been extensively studied for correlations with metastasis and organ colonization (Turner, 1982;Nicolson, 1984).Observation and measurement of adhesion and motility in vivo have inherent difficulties, but these characters can be investigated in vitro and some clues about their possible significance in vivo thereby gained (Briles & Kornfeld, 1978; Hart, 1979;Vollmers & Birchmeier, 1983;McCarthy et al., 1985).We have, therefore, looked at the adhesive and motile properties of tight and loose cells and also examined their cell surfaces by lectin binding to PAGE separated glycoproteins, radio-iodination of proteins and quantitation of sialic acid content. (Sidebottom & Clark, 1983). The cell lines 1G8(6F) and 1G3(4E) were selected from F87.CI.6T2 cells for tight or loose clonal morphology respectively and their in vitro and in vivo properties have been described elsewhere (Clark & Sidebottom, 1984). Cells were maintained in MEM +10% newborn calf serum (Flow) (cMEM) and subcultured when confluent; they were regularly tested for mycoplasma and found to be negative. Wiscm cells were derived from explanted hearts from one day old Wistar rats and were maintained in DMEM + 10% foetal calf serum (Gibco) +10% tryptose phosphate broth (Difco). To prod...

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Section: Aggregation and Disaggregation The Results Insupporting

confidence: 53%

“…The first measured neuraminidase-induced release of labelled sialic acid from cells (Dennis et al, 1982). Fresh medium containing 2 jiCi ml-1 [6-3H]N-acetylmannosamine (sp.…”

Section: Methodsmentioning

confidence: 99%

Morphological and metastatic murine melanoma variants: motility, adhesiveness, cell surface and in vivo properties

Clark¹,

Js²,

Sidebottom³

1987

Br J Cancer

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“…Although alterations in complex O‐glycosylation, N‐glycosylation, and terminal carbohydrate structures were reported to most likely impact the survival and progression of neoplastic cells in some studies,28, 36, 37 no studies have investigated the detailed variations in the distribution of carbohydrates accompanied with tumorigenesis. Herein, based on the core structures of N‐linked and O‐linked oligosaccharides, we selected six common monosaccharides as the investigated targets.…”

Section: Resultsmentioning

confidence: 99%

Variation in Carbohydrates between Cancer and Normal Cell Membranes Revealed by Super‐Resolution Fluorescence Imaging

et al. 2016

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Carbohydrate alterations on cell membranes are associated with various cancer processes, including tumorigenesis, malignant transformation, and tumor dissemination. However, variations in the distributions of cancer‐associated carbohydrates are unclear at the molecular level. Herein, direct stochastic optical reconstruction microscopy is used to reveal that seven major types of carbohydrates tended to form obvious clusters on cancer cell membranes compared with normal cell membranes (both cultured and primary cells), and most types of carbohydrates present a similar distributed characteristic on various cancer cells (e.g., HeLa and Os‐Rc‐2 cells). Significantly, sialic acid is found to distribute in larger‐sized clusters with a higher cluster coverage percentage on various cancer cells than normal cells. These findings on the aberrant distributions of cancer‐associated carbohydrates can potentially serve as novel diagnostic and therapeutic targets, as well as making a contribution to clarify how abnormal glycosylations of membrane glycoconjugates participate in tumorigenesis and metastasis.

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“…In this way neutrophils can be recruited to sites of inflammation. However, sL X and sL A are known to also be expressed on a number of different tumour cell types and for many years this interaction has been implicated in the pathogenesis of cancer metastasis (Brodt et al, 1997;Dennis et al, 1982;Kitayama et al, 2000). SL X expression is increased in human hepatic colorectal metastases compared to the primary tumour (Hoff et al, 1989) and expression has been shown to correlate with poor survival of colorectal cancer patients (for example, in stage III patients 5 year survival was 42% in the sL X positive group vs 81% in patients with tumours negative for sL X in one study) (Nakamori et al, 1993).…”

mentioning

confidence: 99%

Cimetidine in colorectal cancer – are the effects immunological or adhesion-mediated?

Eaton

Hawkins

2002

Br J Cancer

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Surface sialic acid reduces attachment of metastatic tumour cells to collagen type IV and fibronectin

Cited by 204 publications

References 24 publications

Morphological and metastatic murine melanoma variants: motility, adhesiveness, cell surface and in vivo properties

Morphological and metastatic murine melanoma variants: motility, adhesiveness, cell surface and in vivo properties

Variation in Carbohydrates between Cancer and Normal Cell Membranes Revealed by Super‐Resolution Fluorescence Imaging

Cimetidine in colorectal cancer – are the effects immunological or adhesion-mediated?

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