Effect of enzymic removal of cell surface constituents on metastatic colonisation potential of mouse mammary tumour cells

Sargent, N. S. E.; Price, Janet E.; Tarin, David

doi:10.1038/bjc.1983.230

Cited by 16 publications

(10 citation statements)

References 29 publications

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“…The observations are supported by those published earlier (Sargent et al, 1983) demonstrating that vigorous digestion of surface components by various enzymes did not have striking effects on colonisation capability by similar murine mammary tumour cells. In the current work the most marked effect on pulmonary Irimura and Nicolson (1982).…”

Section: Discussionsupporting

confidence: 81%

Effects of altering surface glycoprotein composition on metastatic colonisation potential of murine mammary tumour cells

Sargent¹,

Price²,

Darling³

et al. 1987

Br J Cancer

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Summary This study has examinied cells from naturally-occurring murine mammary tumours to ascertain whether cell surface glycoproteins play a significant role in colonisation of the lungs after intravenous inoculation. It was found that gel electrophoretic analysis of membrane extracts and lectin adsorption studies (ild inot reve;fl anv consistent differences in dlvconrotein composition of cells from tumours which can heavily colonise the lungs relative to ones from tumours which . innot do so or to cells from pulmonary metastases. Also, alteration of structural and functional properties of surface glycoproteins by treatment with succinylated lectins or with drugs such as tunicamycin and swainsonine, which inhibit glycosylation of membrane proteins, had no specific effects on metastatic colonisation of the lungs. Tunicamycin apparently decreased capability to form experimental metastases but also diminished tumourigenicity on subcutaneous inoculation, although it did not affect tumour cell viability in vitro. This information supports earlier studies from this laboratory involving enzymic digestion of the surface of living tumour cells before inoculation and demonstrates that the pulmonary colonisation capability of these mammary tumour cells can withstand global disorganisation of membrane glycoprotein structure and composition. This implies that either the surface glycoproteins are not important in the colonisation process, or that these tumour cells have great capability for rapid repair of their surfaces. It is concluded that a clear answer to whether surface glycoprotein composition has a decisive role in pulmonary colonisation by these mammary tumour cells requires introduction of stable heritable traits into tumour cell populations by genetic manipulation.

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Section: Discussionsupporting

confidence: 81%

Effects of altering surface glycoprotein composition on metastatic colonisation potential of murine mammary tumour cells

Sargent¹,

Price²,

Darling³

et al. 1987

Br J Cancer

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“…Experimental induction of MHC molecules in some tumour cell lines lacking in these determinants has demonstrated the involvement of immune phenomena in modulating metastatic spread (Hui et al, 1984;Wallich et al, 1985). Other cell surface molecular differences between metastatic and nonmetastatic tumour variants are thought to affect cell-cell and cell-tissue interactions influencing adhesiveness and organ colonising properties of tumour cells (Reiber & Reiber, 1981;Sargent et al, 1983). Non-specific defence mechanisms have also been shown to control tumour cell dissemination (Barlozzari et al, 1985).…”

Section: Discussionmentioning

confidence: 99%

“…Quantitative differences in terminal cell surface carbohydrates (Fogl et al, 1983), altered cell surface protein composition after enzyme treatment (Sargent et al, 1983) and differences in glycoprotein expression (Altevogt et al, 1982) have all been shown to contribute to the metastatic capacity of different tumour cell lines. The most notable finding to date is an inverse correlation between metastatic potential and the expression of major histocompatibility complex (MHC) molecules (Wallich et al, 1985;Hui et al, 1984;Albino et al, 1981;Natali et al, 1983).…”

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confidence: 99%

Modulation and biological effects of Ly-6.2 expression on EL4 tumour cells

Matossian-Rogers

Rogers²

1987

Br J Cancer

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Summary EL4 tumour cells maintained in culture were separated by FACS analysis to Ly-6.2 negative and Ly-6.2 positive subsets. The Ly-6.2 negative subset gained expression of this determinant on repeated in vivo passage in C57BL/6 mice. Both subsets injected intraperitoneally or intramuscularly in syngeneic mice induced identical changes in lymphocyte profiles. There was generalised lymphocytolysis in both T-and B-cell compartments. The Lyt-l +, 2-T-lymphocytes were more susceptible to cytolysis causing an alteration of the proportional representation of the Lyt-2+ subset from 30% of splenic T-cells Tumour cell populations are heterogeneous with respect to a variety of properties that influence their growth and survival in the host (Poste & Fidler, 1980;Nicholson, 1984). Development of heterogeneity is thought to be part of the tumorigenic process causing the progression of primary tumours from the benign to the malignant state (Harris et al., 1982;Fidler & Hart, 1982). This may involve the selection of stable subpopulations of cells in the original tumour which possess intrinsic properties that promote dissemination; it may also reflect the acquisition of such properties due to genetic alterations that may arise under the influence of selective pressures of the host response (Layton & Franks, 1984;Bernstein & Weinberg, 1985).Comparative examinations of metastatic variants and parental tumour lines have centred on the study of cell surface compositions of neoplastic cell lines. Quantitative differences in terminal cell surface carbohydrates (Fogl et al., 1983), altered cell surface protein composition after enzyme treatment (Sargent et al., 1983) and differences in glycoprotein expression (Altevogt et al., 1982) have all been shown to contribute to the metastatic capacity of different tumour cell lines. The most notable finding to date is an inverse correlation between metastatic potential and the expression of major histocompatibility complex (MHC) molecules (Wallich et al., 1985;Hui et al., 1984;Albino et al., 1981;Natali et al., 1983).In this study we demonstrate that in the EL4 murine Tcell leukaemia model there is a direct relationship between expression of the lymphocyte differentiation antigen Ly-6.2 and dissemination of the tumour cells to the spleen and lymph nodes from an intramuscular site. EL4 tumour cells maintained in culture are heterogeneous with respect to Ly-6.2 expression. Tumour cells selected by fluorescence activated cell sorter (FACS) analysis on the basis of lack of expression of Ly-6.2, gained this determinant on in vivo passage while parallel in vitro cultures remained negative. To determine the biological effects of Ly-6.2 expression on EL4 tumour cells, Ly-6.2-and Ly-6.2+ tumour cells were injected into syngeneic C57BL/6 mice and their effects on lymphocyte profiles and capacity to metastasize into the lymphoid organs examined. as a second step reagent. Monoclonal antibodies against Thy-I and Lyt-2 were derived from hybridoma clones 53-2.1 and 53-6.7 respectively (Ledbetter & Her...

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“…In addition, preclinical data obtained in cell culture (Liu et al 1987;Kohno et al 1988;Scheithauer et al 1988;Lehnert et al 1989) and experimental rodent tumour models (Seipelt and Kohlheb 1967;Pawlowski et al 1979;Sargent et al 1983) are scanty and inconsistent.…”

Section: Introductionmentioning

confidence: 99%

Hyaluronidase enhances the activity of Adriamycin in breast cancer models in vitro and in vivo

Beckenlehner

Bannke

Spruß

et al. 1992

J Cancer Res Clin Oncol

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Summary.The effect ofhyaluronidase and a combination of hyaluronidase with Adriamycin was investigated on several breast cancer models in vitro and in vivo. In vitro enzyme treatment (using concentrations up to 80 000 IU/ 1) of routine (MXT-, MXT -+, and MXT +) and human (MCF-7, ZR-75-1 and T-47-D) breast cancer cell lines did not inhibit tumour cell proliferation (measured by a kinetic crystal violet assay) in either case. Although highdose hyaluronidase (1.2 x 106 IU/kg) was ineffective, when administered peritumourally to the MXT M3.2 mammary carcinoma of the B6D2F 1 mouse, it is remarkable that five "megadoses" were excellently tolerated. However, the antineoplastic activity of Adriamycin against the oestrogen-receptor-positive variant of the MXT tumour was significantly enhanced by combination with concentrations of hyaluronidase that were inactive per se, both in vitro and in vivo. Interestingly, the enhancement of the in vivo antitumour activity was not compromised by toxic side-effects.

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Effect of enzymic removal of cell surface constituents on metastatic colonisation potential of mouse mammary tumour cells

Abstract: Clinical observations indicate that individual tumours vary in the extent to which they colonise distant organs and in the distribution of their metastatic deposits after blood-borne dissemination.

Cited by 16 publications

References 29 publications

Effects of altering surface glycoprotein composition on metastatic colonisation potential of murine mammary tumour cells

Effects of altering surface glycoprotein composition on metastatic colonisation potential of murine mammary tumour cells

Modulation and biological effects of Ly-6.2 expression on EL4 tumour cells

Hyaluronidase enhances the activity of Adriamycin in breast cancer models in vitro and in vivo

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