Drug-Induced Tumor Progression in a Rat Rhabdomyosarcoma

Pauwels, C; Antoine, Etienne; Nolibé, D.; Lascaux,; Boyano, L; Hanania, Nicole; Mf, Poupon

doi:10.1007/978-1-4899-5037-6_42

Cited by 2 publications

(2 citation statements)

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“…The differences in glycan expression between S4MH and F21 cells may be explained by differences in the expression of certain genes. Thus, previous studies have demonstrated that, in comparison with F21 cells, S4MH cells overexpress the c-myc and Ha-ras oncogenes [37], which have been postulated to induce the overexpression of ß1-6 branched oligosaccharides [44][45][46]. Flow cytometry analyses after treatment of S4MH tumor cells with tunicamycin or BzGalNAc, inhibitors of N-and O-glycosylation, respectively, permitted us to establish that the carbohydrate structures recognized by PHA-L and WGA were mainly located on N-glycans of S4MH cells.…”

Section: Discussionmentioning

confidence: 99%

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Tunicamycin Treatment Reduces Intracellular Glutathione Levels: Effect on the Metastatic Potential of the Rhabdomyosarcoma Cell Line S4MH

et al. 2000

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Highly metastatic cells are known to overexpress certain Asn-linked oligosaccharides in the plasmatic membrane. Another phenotypic characteristic of malignant cells consists in the expression of high levels of intracellular glutathione (GSH). The aim of the present work was to demonstrate that the inhibition of N-glycosylation induces changes in intracellular GSH levels, and in turn participates in the inhibition of the metastatic potential of tumor cells by tunicamycin treatment. Firstly, we demonstrated that in comparison to the poorly metastatic cell line F21, the highly metastatic cells S4MH express a higher number of Asn-linked β1–6 branched oligosaccharides and sialic acid (SA) and/or chitobiose oligosaccharides in glycoproteins involved in the regulation of the adhesion efficiency of tumor cells on endothelial cells and extracellular matrix. Our results showed that the decrease in S4MH cell adhesion efficiency on endothelial cells and extracellular matrix after the inhibition of N-glycan processing by tunicamycin treatment was caused by: (1) inhibition of the expression of N-glycan structures recognized by endothelial endogenous lectins, including β1–6 branched oligosaccharides and SA and/or chitobiose oligosaccharides, and (2) redistribution of cell surface glycoproteins with β1–6 branched oligosaccharides and/or SA and/or chitobiose oligosaccharides in their structures, caused by the depletion of intracellular GSH levels. The latter condition prevents the organization of these glycoproteins in the plasmatic membrane of S4MH cells necessary for anchoring to the substratum.

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Section: Discussionmentioning

confidence: 99%

“…Two variants from the same parental rhabdomyosarcoma cell line with different metastatic potential were used: S4MH (highly metastatic) and F21 (poorly metastatic) [37,38]. The cells were maintained in tissue culture in Dulbecco's minimum essential medium (DMEM) and supplemented with 15 and 10% fetal bovine serum (FBS), respectively.…”

Section: Tumor Cell Linesmentioning

confidence: 99%