An inverse correlation between expression of NCAM-A and the matrix-metalloproteinases gelatinase-A and gelatinase-B in human glioma cells in vitro

Maidment, Stephen L; Rucklidge, Garry J.; Rooprai, Harcharan K.; Pilkington, Geoffrey J.

doi:10.1016/s0304-3835(97)00171-7

Cited by 24 publications

(12 citation statements)

References 24 publications

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“…43 Two of the MMPs that have been implicated in glioma invasiveness are MMP-2 and MMP-9, 44 -46 and these have been shown to be regulated by expression of CAMs. 47,48 Gelatin zymography did not show any difference in the levels of MMP-2 or MMP-9, or any other gelatinases, in the 3 cell populations described in our study (data not shown). The transcript levels of the tissue inhibitors of MMPs, TIMP-1 to TIMP-4, were also not changed between the cell populations (data not shown).…”

Section: Discussionmentioning

confidence: 47%

Impact of the coxsackie and adenovirus receptor (CAR) on glioma cell growth and invasion: Requirement for the C‐terminal domain

Huang

Altinöz

Wosik

et al. 2004

Intl Journal of Cancer

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Expression of the coxsackie and adenovirus receptor (CAR) is downregulated in malignant glioma cell lines and is barely detectable in high-grade primary astrocytoma (glioblastoma multiforme). We determined the effect of forced CAR expression on the invasion and growth of the human glioma cell line U87-MG, which does not express any CAR. Although retrovirally mediated expression of full-length CAR in U87-MG cells did not affect monolayer growth in vitro, it did reduce glioma cell invasion in a 3-dimensional spheroid model. Furthermore, in xenograft experiments, intracerebral implantation of glioma cells expressing full-length CAR resulted in tumors with a significantly reduced volume compared to tumors generated by control vector-transduced U87-MG cells. In contrast, U87-MG cells expressing transmembrane CAR with a deletion of the entire cytoplasmic domain (except for the first 2 intracellular juxtamembrane cysteine amino acids) had rates of invasion and tumor growth that were similar to those of the control cells. This difference in behavior between the 2 forms of CAR was not due to improper cell surface localization of the cytoplasmically deleted CAR as determined by comparable immunostaining of unpermeabilized cells, equivalent adenoviral transduction of the cells and similar extent of fractionation into lipidrich domains. Taken together, these results suggest that the decrease or loss of CAR expression in malignant glioma may confer a selective advantage in growth and invasion to these tumors.

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Section: Discussionmentioning

confidence: 47%

Impact of the coxsackie and adenovirus receptor (CAR) on glioma cell growth and invasion: Requirement for the C‐terminal domain

Huang

Altinöz

Wosik

et al. 2004

Intl Journal of Cancer

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“…It has been shown in culture that N-CAM, is downregulated in the migratory phase of brain tumor invasion to promote cell disaggregation and, furthermore, shows an inverse correlation with ganglioside as well as metalloproteinase expression facilitating migration [57][58][59][60]. Regarding individual patients and tumors in this study, there was no correlation between expression of N-CAM and MMP-2 and MMP-9.…”

Section: Discussionmentioning

confidence: 67%

Expression of Adhesion Factors and Degrading Proteins in Primary and Secondary Glioblastomas and Their Precursor Tumors

Tews

Nissen²

1998

Invasion Metastasis

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In tumor tissue specimens of 27 primary and 17 secondary glioblastomas and the precursor lesions, the immunohistochemical expression patterns of the membrane protein CD44s, the basal lamina proteins laminin, collagen IV, and fibronectin, the lectin galectin-3 recognizing tenascin and N-CAM as well as of the matrix-degrading enzymes matrix metalloproteinase MMP-2 and MMP-9, and cathepsin D were studied. Besides expression of basal lamina proteins in vessels, all glioblastomas and the precursor lesions showed strong immunoreactivity of CD44s, tenascin, galectin-3, and N-CAM which were restricted to solid tumor masses. Present in solid tumor areas, MMP-2, MMP-9 and cathepsin D were also strongly expressed by single tumors cells invading adjacent brain tissue at the infiltrative margin. Neither the expression pattern in primary and secondary glioblastomas nor in the precursor tumors revealed significant differences. There was also no intraindividual constant expression pattern during glioma progression or correlation with malignancy. Restricted expression of CD44s, galectin-3, tenascin and N-CAM in solid tumor masses seems to contribute to homotypic tumor cell adhesion while single tumor cells abolish this expression profile and acquire invasive activities by expression of cathepsin D, MMP-2 and MMP-9.

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“…Prior studies showed that NCAM-140 is reduced during migration and proliferation of glioma cells while the matrix metalloproteinases are increased (Edvardsen et al 1993b;Maidment et al 1997;Gratsa et al 1997). One could assume that this is the reason, why gliomas loose NCAM-140 with rising WHO grade.…”

Section: Discussionmentioning

confidence: 99%

Neural cell adhesion molecule isoform 140 declines with rise of WHO grade in human gliomas and serves as indicator for the invasion zone of multiform glioblastomas and brain metastases

Duenisch

Reichart

Mueller³

et al. 2010

J Cancer Res Clin Oncol

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An inverse correlation between expression of NCAM-A and the matrix-metalloproteinases gelatinase-A and gelatinase-B in human glioma cells in vitro

Cited by 24 publications

References 24 publications

Impact of the coxsackie and adenovirus receptor (CAR) on glioma cell growth and invasion: Requirement for the C‐terminal domain

Impact of the coxsackie and adenovirus receptor (CAR) on glioma cell growth and invasion: Requirement for the C‐terminal domain

Expression of Adhesion Factors and Degrading Proteins in Primary and Secondary Glioblastomas and Their Precursor Tumors

Neural cell adhesion molecule isoform 140 declines with rise of WHO grade in human gliomas and serves as indicator for the invasion zone of multiform glioblastomas and brain metastases

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