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  • 1
    Electronic Resource
    Electronic Resource
    Inhibition of VLA-4 and up-regulation of TIMP-1 expression in B16BL6 melanoma cells transfected with MHC class I genes (1998)
    Springer
    Clinical & experimental metastasis 16 (1998), S. 358-370 
    Details
    ISSN: 1573-7276
    Keywords: metastasis ; MHC class I genes ; TIMP-1 ; VLA-4
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of MHC class I gene transfection on the metastatic properties of B16BL6 melanoma cells was investigated. BL6-8 melanoma cells transfected with H-2K or H-2K, but not H-2D or H-2L, genes showed a dramatic reduction in their ability to generate experimental metastases in immunosuppressed CB6F1 mice. This observation suggested that some changes in the metastatic phenotype may have been induced in the H-2K- transfected melanoma cells. Analyses of adhesive and invasive properties of BL6-8 melanoma cells transfected with H-2 class I genes have been performed. We found that the loss of metastatic properties in the H-2K or H-2K gene-transfected melanoma cells was associated with reduced adherence to endothe-lial cells, laminin and collagen IV, decreased ability to form homotypic cell aggregates and with a complete loss of VLA-4 integrin expression. In addition, BL6-8 melanoma cells transfected with H-2K genes demon-strated reduced ability to invade Matrigel that paralleled up -regulation of TIMP-1 expression. Incubation of untransfected BL6-8 clone or B16F1 cells with 5-azacytidine similarly resulted in up-regulation of TIMP-1, suggesting that the changes in methylation of TIMP-1 gene could be responsible for TIMP-1 expression in the H-2K-transfected BL6-8 melanoma cells. Transfection of BL6-8 cells with the H-2D d /L d genes did not affect their adhesive and invasive properties. Previously we reported that reduction in the metastatic properties of the H-2K b transfected cells was associated with alterations in cell surface carbohydrates with appearance of a-galactosyl epitopes and reduction in cell surface sialylation. The present data indicate that, in addition to changes in cell surface carbohydrates, reduction in adhesive properties and up-regulation of TIMP-1 may be responsible for the observed loss of metastatic potential of BL6-8 cells transfected with the H-2K genes. © Rapid Science Ltd.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006569631330
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  • 2
    Electronic Resource
    Electronic Resource
    Expression of bone sialoprotein and osteopontin in breast cancer bone metastases (2000)
    Springer
    Clinical & experimental metastasis 18 (2000), S. 253-260 
    Details
    ISSN: 1573-7276
    Keywords: bone sialoprotein ; osteopontin ; breast cancer ; metastasis ; bone metastases ; immunohistochemistry ; in situ hybridization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Bone sialoprotein (BSP) and osteopontin (OPN) are prominent, mineral-associated proteins in the extracellular matrix of bone that have been implicated in the metastatic activity of cancer cells. The expression of BSP, which is normally restricted to mineralizing tissues, has been observed in cancers with a high propensity for forming bone metastases. To investigate the relationship between BSP expression and the formation of bone metastases we have conducted an initial study of the expression of BSP in 10 intraductal breast carcinoma bone metastases using immunostaining and in situ hybridization, and compared the expression with OPN. The metastases were characterized by the infiltration of tumour cells into bone with extensive bone resorption evident. Moderate to strong staining for BSP was observed in all (100%) carcinomas, which also expressed BSP mRNA as determined by in situ hybridization. Variable staining for BSP was also observed in the mineralized bone and expression of BSP mRNA could be observed in osteoblastic cells on the bone surface and in some osteocytes at sites of bone remodelling. Contrary to a previous report, BSP expression could be demonstrated by PCR in three breast cancer cell lines, MCF-7, T47-D and MDA-MB-231. Moreover, in sub-cutaneous tumours formed by MDA-MB-231 breast cancer cells injected into athymic mice, higher immunostaining for BSP was seen in large ulcerating tumours in which mineral deposits were formed. In contrast to BSP, staining for OPN in bone metastases was generally restricted to the interface between tumor cells and bone surface of the carcinomas. While OPN staining was also observed in the cytoplasm of osteoclasts, which showed strong hybridization to a digoxygenin-labelled OPN cRNA probe, expression of OPN was not clearly detectable in the tumour cells. These studies provide the first demonstration of BSP expression by tumour cells in bone metastases and support the concept that BSP may have a role in targeting metastatic cells to bone. Expression of OPN in bone metastases appears to be related to increased bone resorptive activity by osteoclasts.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006754605901
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  • 3
    Electronic Resource
    Electronic Resource
    Mechanisms involved in the metastasis of cancer to bone (1993)
    Springer
    Breast cancer research and treatment 25 (1993), S. 151-163 
    Details
    ISSN: 1573-7217
    Keywords: bone metastasis ; growth factors ; microenvironment ; osteolysis ; TGF-β ; Walker 256 rat cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The metastasis of cancer to bone is a frequent outcome of common malignancies and is often associated with significant morbidity due to osteolysis. Bone metastasis is also selective in that a disproportionately small number of malignancies account for the majority of tumors which spread to bone. While the mechanisms of bone destruction have been studied, those responsible for the site-specific nature of bone metastasis are poorly understood. As a metastatic target, bone is unique in that it is continuously being remodelled under the influence of local and systemic growth factors, many of which are embedded in the bone matrix. This review summarizes evidence for the hypothesis that the formation of metastatic tumors in bone is the consequence of a unique microenvironment where metastatic cells can alter the metabolism of bone, thereby regulating the release of soluble bone-derived growth factors as a consequence of bone resorption. These, in turn, can modulate the malignant phenotypic properties of receptive cells. Transforming growth factor-β is one factor which can promote the growth and motility of Walker 256 cells, a rat cell line with a propensity to metastasize spontaneously to bone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00662140
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    Paper (German National Licenses)
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