Adhesion characteristics of human melanoma cell lines of varying metastatic potential

Ej, Ormerod; Ca, Everett; Ir, Hart

doi:10.1002/ijc.2910410126

Cited by 15 publications

(7 citation statements)

References 15 publications

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“…The percentages of tumor cells bound to endothelial cell monolayers and to ECM were similar to those obtained by Vlodavsky et al [23]. Comparison between the two variants showed that a lower percentage of the HM than of the LM cells were able to attach to ABAE cells as well as to ECM: TAU-39 cells attached 160 Klci n/Sav ion/Staroselsky/Leibov ici Metastatic Capacity and Adhesion to Endothelial Cells and ECM [35][36][37], other groups found no differences in adherence capacity between variants of malignancy [38] and others have found results similar to ours, namely a preferential adherence ability to endothelial monolayers and ECM of LM than of HM tumor cells [39], A possible interpretation of the higher attachment of LM compared to HM cells to endothelial cells and their ECM could be that tumor cells should be able not only to attach to these host barriers but also to detach from them, in order to be able to continue their spread to the target organs. It is possible indeed that the capacity of the tumor cells to detach from the blood vessel barrier facilitates the extravasation step and the two lymphoma variants differ at this particular stage.…”

Section: Discussionsupporting

confidence: 71%

Cellular Functions Related to Metastasis Differing between Low- and High-Malignancy Variants of AKR Lymphoma

Klein

Savion²,

Staroselsky³

et al. 1992

Pathobiology

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Two AKR lymphoma variants of low (LM) and high (HM) malignancy were characterized for cell properties important for metastatic capacity. Previous data suggested that these murine lymphoma variants differed in the late phase of metastasis. In the present study we attempted to determine more accurately the stage in which they differ. The HM cells attached less efficiently than the LM ones to both endothelial cells (5 times) and extracellular matrix (twice), possibly indicating a more efficient extravasation capacity of the HM cells. The level of heparinase was low in the two variant cells. Attachment to liver sections was, however, more efficient with the HM than with the LM cells.

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Section: Discussionsupporting

confidence: 71%

Cellular Functions Related to Metastasis Differing between Low- and High-Malignancy Variants of AKR Lymphoma

Klein

Savion²,

Staroselsky³

et al. 1992

Pathobiology

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“…These results are inconsistent with most, but not all [36,37] previous studies, showing that highly metastatic cells possessed greater preferential adhesion affinities to purified FN, LN, or CL-IV substrates [13,[38][39][40][41] or vascular endothelial cell ECM [42,43] than weakly metastatic cells.…”

Section: Discussioncontrasting

confidence: 56%

Substrate adhesiveness and experimental metastatic potential of rat ascites hepatoma AH7974-derived variant sublines

et al. 1992

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Cells of an adherent subline (74AD, adhesion greater than 95%) and a floating subline (74FL, adhesion less than 1%) of rat ascites hepatoma AH7974 produced substrates containing fibronectin (FN), laminin (LN) and type IV collagen (CL-IV), with 74AD cells producing higher levels of each component. 74AD cells possessed high adhesion affinities to LN and CL-IV substrates. By contrast, 74FL cells hardly adhered to these purified attachment proteins. The difference in adhesion between the two lines in vitro tended to increase on incubation of the cells in medium containing fetal bovine serum. However, 74FL and 74AD cells adhered avidly to the extracellular matrix (ECM) of vascular endothelial cells. Although the cell-ECM adhesion apparently was not inhibited by pretreatment of the ECM with anti-FN, anti-LN and anti-CL-IV antibodies, the 74FL cell-ECM adhesion was inhibited considerably by pretreatment of the ECM with a mixture of these antibodies, especially with a combination of anti-FN and anti-LN antibodies. The lung-colonizing potential of 74FL cells was greater than that of 74AD cells, but the liver-colonizing potential of 74FL cells was less than that of 74AD cells. These results suggest that rat ascites hepatoma cells with extremely reduced substrate adhesiveness retain an adhesion mechanism that binds to FN and LN in the ECM of vascular endothelial cells. This mechanism may be a minimum essential unit of tumor cell-ECM adhesion in lung colonization, but the unit is insufficient for liver colonization of these cells.

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“…G antigen 7 is expressed in prostate cancer (43), and G antigen 7c was proposed to be an antiapoptotic gene (57). Similarly, MAGE expression is associated with metastasis (53,54). SSX2 was shown to be expressed in a wide variety of tumors (50) and was identified as one of 13 antigens that react exclusively with sera from colon cancer patients but not with sera from normal patients (58).…”

Section: Discussionmentioning

confidence: 99%

Epigenomic Stress Response

Milutinovic

Zhuang

Niveleau

et al. 2003

Journal of Biological Chemistry

109

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The DNA methylation pattern is an important component of the epigenome that regulates and maintains gene expression programs. In this paper, we test the hypothesis that vertebrate cells possess mechanisms protecting them from epigenomic stress similar to DNA damage checkpoints. We show that knockdown of DNMT1 (DNA methyltransferase 1) by an antisense oligonucleotide triggers an intra-S-phase arrest of DNA replication that is not observed with control oligonucleotide. The cells are arrested at different positions throughout the S-phase of the cell cycle, suggesting that this response is not specific to distinct classes of origins of replication. The intra-S-phase arrest of DNA replication is proposed to protect the genome from extensive DNA demethylation that could come about by replication in the absence of DNMT1. This protective mechanism is not induced by 5-aza-2 -deoxycytidine, a nucleoside analog that inhibits DNA methylation by trapping DNMT1 in the progressing replication fork, but does not reduce de novo synthesis of DNMT1. Our data therefore suggest that the intra-S-phase arrest is triggered by a reduction in DNMT1 and not by demethylation of DNA. DNMT1 knockdown also leads to an induction of a set of genes that are implicated in genotoxic stress response such as NF-B, JunB, ATF-3, and GADD45␤ (growth arrest DNA damage 45␤ gene). Based on these data, we suggest that this stress response mechanism evolved to guard against buildup of DNA methylation errors and to coordinate inheritance of genomic and epigenomic information.Proper epigenomic regulation of gene expression is essential for the integrity of cell function. One critical component of the epigenome is the pattern of distribution of methylated cytosines in CG dinucleotide sequences in the genome (1). Methylation of CGs marks genes for inactivation by either interfering with the binding of methylated DNA-sensitive transcription factors (2) or by recruiting methylated DNA-binding proteins such as MeCP2, which in turn recruit corepressor complexes and histone deacetylases to the chromatin associated with the gene (3). The methylation pattern can thus determine the chromatin structure and state of activity of genes. Disruption in the proper maintenance of the DNA methylation pattern results in aberrant gene expression, as is observed in tumor suppressor genes that are hypermethylated in cancer (4). Aberrant hypomethylation can also result in improper activation of genes (5).The main enzyme responsible for replicating the DNA methylation pattern is DNMT1 (DNA methyltransferase 1). This enzyme shows preference for hemimethylated DNA and is therefore believed to faithfully copy the DNA methylation pattern (6). Multiple mechanisms have been proposed to coordinate the inheritance of DNA methylation patterns with DNA replication. First, DNMT1 expression is regulated with the cell cycle (7, 8), and it is up-regulated by proto-oncogenes Ras and Jun (9 -11), Fos (12), and T antigen (13). Second, DNMT1 is localized to the replication fork (14) and is associated ...

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Adhesion characteristics of human melanoma cell lines of varying metastatic potential

Cited by 15 publications

References 15 publications

Cellular Functions Related to Metastasis Differing between Low- and High-Malignancy Variants of AKR Lymphoma

Cellular Functions Related to Metastasis Differing between Low- and High-Malignancy Variants of AKR Lymphoma

Substrate adhesiveness and experimental metastatic potential of rat ascites hepatoma AH7974-derived variant sublines

Epigenomic Stress Response

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