The identification of a neutral glycosphingolipid antigenic marker for metastatic cells in the R3230AC rat mammary adenocarcinoma

Carlsen, Svein A.; Barry, Michele M.; Newton, Karen

doi:10.1007/bf00117787

Cited by 7 publications

(10 citation statements)

References 16 publications

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“…Our laboratory has established a rat mammary tumor model where highly and poorly metastatic subpopulations, termed R3230Ac-LN 4 and R3230Ac-CAb, respectively, have been derived from the same R3230Ac rat mammary adenocarcinoma (21,30,32). In the experiments described in this paper, clonal isolates of these two cell populations, LN4D6 and CAbD5, were used.…”

Section: Resultsmentioning

confidence: 99%

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CREB3L1 Is a Metastasis Suppressor That Represses Expression of Genes Regulating Metastasis, Invasion, and Angiogenesis

Mellor

Deibert

Calvert

et al. 2013

Molecular and Cellular Biology

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The unfolded protein response (UPR) is activated in response to hypoxia-induced stress such as in the tumor microenvironment. This study examined the role of CREB3L1 (cyclic AMP [cAMP]-responsive element-binding protein 3-like protein 1), a member of the UPR, in breast cancer development and metastasis. Initial experiments identified the loss of CREB3L1 expression in metastatic breast cancer cell lines compared to low-metastasis or nonmetastatic cell lines. When metastatic cells were transfected with CREB3L1, they demonstrated reduced invasion and migration in vitro, as well as a significantly decreased ability to survive under nonadherent or hypoxic conditions. Interestingly, in an in vivo rat mammary tumor model, not only did CREB3L1-expressing cells fail to form metastases compared to CREB3L1 null cells but regression of the primary tumors was seen in 70% of the animals as a result of impaired angiogenesis. Microarray and chromatin immunoprecipitation with microarray technology (ChIP on Chip) analyses identified changes in the expression of many genes involved in cancer development and metastasis, including a decrease in those involved in angiogenesis. These data suggest that CREB3L1 plays an important role in suppressing tumorigenesis and that loss of expression is required for the development of a metastatic phenotype.

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Section: Resultsmentioning

confidence: 99%

“…Our laboratory has established a rat mammary tumor model where highly (LN4D6) and poorly (CAbD5) metastatic subpopulations have been derived from the R3230Ac rat mammary adenocarcinoma (21). Stable LN4D6ϩpUB6-HA 3 CREB3L1 (LN4D6 CREB3L1) and LN4D6ϩpUB6-HA 3 vector-only (LN4D6 vector) transfected cell lines were generated.…”

Section: Methodsmentioning

confidence: 99%

CREB3L1 Is a Metastasis Suppressor That Represses Expression of Genes Regulating Metastasis, Invasion, and Angiogenesis

Mellor

Deibert

Calvert

et al. 2013

Molecular and Cellular Biology

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“…Relevant in this respect are two recent reports by Carlsen et al which implicate a cell surface soybean agglutinin-binding glycolipid in lymphatic metastasis of a rat mammary adenocarcinoma. Depletion of cells bearing this glycolipid was shown to reduce significantly tumor cell potential to metastasize to the regional lymph nodes [39,40]. Its role in tumor cell adhesion has not, however, been elucidated.…”

Section: The Role Of Other Adhesion Moleculesmentioning

confidence: 99%

Adhesion mechanisms in lymphatic metastasis

Brodt

1991

Cancer Metast Rev

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The role of cellular adhesion in regional lymph node metastasis of solid tumors has been investigated. The data reviewed is based on studies in four different tumor models of human, rat and murine origin. An in vitro assay measuring tumor cell attachment to cryostat sections of normal peripheral lymph nodes, obtained from the species of tumor origin was used to compare the adhesion of tumor sublines with different metastatic potentials. A good correlation was found between tumor cell potential to metastasize to regional nodes and the adhesion to the sections in all models studied. The adhesion of all tumor lines could be blocked by Arg-Gly-Asp containing peptides while pretreatment of the cells with antibodies to integrins implicated beta 1 and beta 3 receptor complexes in the adhesion. Ligand binding assays provided indirect evidence that the preferential attachment of the metastatic tumor lines to the frozen sections was mediated via extracellular matrix proteins such as fibronectin, vitronectin and type IV collagen. As these basement membrane proteins have been localized to the outer surfaces of reticular fibers which are known to permeate the lymph node and trasverse the subcapsular sinus it is postulated that tumor cell attachment to these fibers may facilitate and possibly be required for tumor cell retention and growth in the invaded regional nodes.

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“…Of particular interest in this context are studies examining the range of gene expression in different cells in the population. Carlsen and coworkers [36,37] have demonstrated that the metastatic ability of rat mammary tumor cells is associated with the level of expression of a glycolipid on the cell surface that binds to soya-bean agglutinin (SBA). Thus, cell populations selected for high levels of SBA binding are more metastatic than cell populations with low levels of binding.…”

Section: Metastasismentioning

confidence: 99%

“…Thus, cell populations selected for high levels of SBA binding are more metastatic than cell populations with low levels of binding. Furthermore, these authors have recently shown [37] that deleting the cells with a high expression of the glycolipid using monoclonal antibody and complement-dependent cytolysis resuits in a reduction in the metastatic ability of the cell population.…”

Section: Metastasismentioning

confidence: 99%

Tumor progression: Potential role of unstable genomic changes

Hill

1990

Cancer Metast Rev

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It is generally accepted that the genome of tumor cells is less stable than that of most normal cells, and it has been hypothesized that this genomic instability is probably involved in the process of tumor progression. However, the rate of occurrence of classical spontaneous mutations in tumor cells is too low to account for the rapid changes that can occur during tumor progression. Thus it is likely that other types of changes, such as gene amplification, must be involved in tumor progression. Gene amplification has been extensively studied in relation to the development of drug resistance. Low levels of amplification can occur spontaneously in tumor cell populations, but the amplified genes are lost rapidly unless prolonged selective pressure is applied. This paper argues that unstable increases in the expression of genes, probably as a result of low levels of amplification, may be all that is required for some of the stages in the process of tumor progression. This may be particularly true for the steps involved in metastasis formation. Recent studies have suggested that microenvironmental conditions known to occur in tumors (hypoxia, nutrient deprivation) may induce gene amplification in cells. This suggests the possibility that such conditions could promote tumor progression.

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The identification of a neutral glycosphingolipid antigenic marker for metastatic cells in the R3230AC rat mammary adenocarcinoma

Cited by 7 publications

References 16 publications

CREB3L1 Is a Metastasis Suppressor That Represses Expression of Genes Regulating Metastasis, Invasion, and Angiogenesis

CREB3L1 Is a Metastasis Suppressor That Represses Expression of Genes Regulating Metastasis, Invasion, and Angiogenesis

Adhesion mechanisms in lymphatic metastasis

Tumor progression: Potential role of unstable genomic changes

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