Estradiol Represses the GD3 Synthase Gene ST8SIA1 Expression in Human Breast Cancer Cells by Preventing NFκB Binding to ST8SIA1 Promoter

Bobowski, Marie; Vincent, Audrey; Steenackers, Agata; Colomb, Florent; Seuningen, Isabelle Van; Julien, Sylvain; Delannoy, Philippe

doi:10.1371/journal.pone.0062559

Cited by 32 publications

(35 citation statements)

References 52 publications

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“…Thus, the TNF-mediated regulation of G D3 and G D2 previously described could involve the NF-κB pathway, which promotes proliferative and prosurvival gene expression; and has been implicated in EMT, the process by which cancer cells become more invasive and acquire metastatic potential [106]. Interestingly, our studies recently demonstrated that TNF induces up-regulation of the GD3S gene expression in ER-negative breast cancer cells via NF-κB transcription factor while in ER-positive cells, estradiol represses the TNF-induced up-regulation of GD3S by inhibiting NF-κB nuclear translocation (Figure 4) [105]. This result could explain the higher expression of GD3S in ER-negative breast cancer cells and allows a better understanding of the molecular mechanism leading to the regulation of gangliosides expression by cytokines.…”

Section: Regulation Of Ganglioside Expression By Pro-inflammatory mentioning

confidence: 99%

“…All together these data indicate that the regulation of ganglioside content by cytokines is closely related to the regulation of the GTs involved in ganglioside biosynthesis. In this prospect, the transcriptional regulation of GD3S gene ( ST8SIA1 ), the key enzyme involved in the biosynthesis of b-and c-series gangliosides, has been well described in melanoma, neuroblastoma and breast cancer cells; highlighting a crucial role of NF-κB in activating this gene [103,104,105]. Thus, the TNF-mediated regulation of G D3 and G D2 previously described could involve the NF-κB pathway, which promotes proliferative and prosurvival gene expression; and has been implicated in EMT, the process by which cancer cells become more invasive and acquire metastatic potential [106].…”

Section: Regulation Of Ganglioside Expression By Pro-inflammatory mentioning

confidence: 99%

“…GD3S gene ( ST8SIA1 ) transcription is activated by NF-κB pathway upon TNF stimulation, leading, in ER-negative breast cancer cells, to an increased expression of GD3S in the Golgi apparatus and disialoganglioside (G D3 and G D2 ) at the cell surface, increasing cell migration and proliferation. In ER-positive breast cancer cells, estradiol (E2)-ERα complex represses the TNF-induced up-regulation of GD3S by inhibiting NF-κB nuclear translocation [105]. …”

Section: Figurementioning

confidence: 99%

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Role of Cytokine-Induced Glycosylation Changes in Regulating Cell Interactions and Cell Signaling in Inflammatory Diseases and Cancer

Dewald

Colomb

Bobowski-Gerard

et al. 2016

Cells

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Glycosylation is one of the most important modifications of proteins and lipids, and cell surface glycoconjugates are thought to play important roles in a variety of biological functions including cell-cell and cell-substrate interactions, bacterial adhesion, cell immunogenicity and cell signaling. Alterations of glycosylation are observed in number of diseases such as cancer and chronic inflammation. In that context, pro-inflammatory cytokines have been shown to modulate cell surface glycosylation by regulating the expression of glycosyltransferases involved in the biosynthesis of carbohydrate chains. These changes in cell surface glycosylation are also known to regulate cell signaling and could contribute to disease pathogenesis. This review summarizes our current knowledge of the glycosylation changes induced by pro-inflammatory cytokines, with a particular focus on cancer and cystic fibrosis, and their consequences on cell interactions and signaling.

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Section: Regulation Of Ganglioside Expression By Pro-inflammatory mentioning

confidence: 99%

Section: Regulation Of Ganglioside Expression By Pro-inflammatory mentioning

confidence: 99%

Section: Figurementioning

confidence: 99%

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Role of Cytokine-Induced Glycosylation Changes in Regulating Cell Interactions and Cell Signaling in Inflammatory Diseases and Cancer

Dewald

Colomb

Bobowski-Gerard

et al. 2016

Cells

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“…Epigenetic control is supposed to be relevant in many cases [47,48], while other emerging mechanisms controlling gene expression, such as the presence of regulatory RNA sequence and or RNA binding proteins [49], are, as yet, unexplored. At present, data are available about promoter sequences and potential regulatory elements operating in various tissues [50,51,52,53,54,55,56,57], while those actually involved in gastrointestinal cancer are described in very few cases [43,58,59,60,61]. This is a very promising field of research since a bidirectional relationship may exist between the expression of sLe antigens and the mechanisms controlling cell growth.…”

Section: Regulation Of Slea and Slexmentioning

confidence: 99%

Selectin Ligands Sialyl-Lewis a and Sialyl-Lewis x in Gastrointestinal Cancers

Trinchera

Aronica

Dall’Olio

2017

Biology

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The tetrasaccharide structures Siaα2,3Galβ1,3(Fucα1,4)GlcNAc and Siaα2,3Galβ1,4(Fucα1,3)GlcNAc constitute the epitopes of the carbohydrate antigens sialyl-Lewis a (sLea) and sialyl-Lewis x (sLex), respectively, and are the minimal requirement for selectin binding to their counter-receptors. Interaction of sLex expressed on the cell surface of leucocytes with E-selectin on endothelial cells allows their arrest and promotes their extravasation. Similarly, the rolling of cancer cells ectopically expressing the selectin ligands on endothelial cells is potentially a crucial step favoring the metastatic process. In this review, we focus on the biosynthetic steps giving rise to selectin ligand expression in cell lines and native tissues of gastrointestinal origin, trying to understand whether and how they are deregulated in cancer. We also discuss the use of such molecules in the diagnosis of gastrointestinal cancers, particularly in light of recent data questioning the ability of colon cancers to express sLea and the possible use of circulating sLex in the early detection of pancreatic cancer. Finally, we reviewed the data dealing with the mechanisms that link selectin ligand expression in gastrointestinal cells to cancer malignancy. This promising research field seems to require additional data on native patient tissues to reach more definitive conclusions.

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“…On the other hand, analysis of cell surface gangliosides in melanocytes incubated with TNF shows a higher expression of GM3 and GD3 [22]. Interestingly, TNF induces up-regulation of the GD3 synthase gene expression in ER-negative breast cancer cells via NFκB transcription factor, while in ER-positive cells, estradiol represses the TNF-induced up-regulation of GD3 synthase by inhibiting NFκB nuclear translocation [23]. Finally, GTs involved in the synthesis of gangliosides can be also regulated by post-translational modifications such as phosphorylation and dephosphorylation [24,25].…”

Section: Introductionmentioning

confidence: 98%

O-acetylated Gangliosides as Targets for Cancer Immunotherapy

Cavdarli

Delannoy

Groux-Degroote

2020

Cells

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O-acetylation of sialic acid residues is one of the main modifications of gangliosides, and modulates ganglioside functions.O-acetylation of gangliosides is dependent on sialyl-O-acetyltransferases and sialyl-O-acetyl-esterase activities. CAS1 Domain-Containing Protein 1 (CASD1) is the only human sialyl-O-acetyltransferases (SOAT) described until now. O-acetylated ganglioside species are mainly expressed during embryonic development and in the central nervous system in healthy adults, but are re-expressed during cancer development and are considered as markers of cancers of neuroectodermal origin. However, the specific biological roles of O-acetylated gangliosides in developing and malignant tissues have not been extensively studied, mostly because of the requirement of specific approaches and tools for sample preparation and analysis. In this review, we summarize our current knowledge of ganglioside biosynthesis and expression in normal and pathological conditions, of ganglioside O-acetylation analysis and expression in cancers, and of the possible use of O-acetylated gangliosides as targets for cancer immunotherapy. a potential functional significance of ganglioside O-acetylation in cancer. The use of O-acetylated gangliosides as targets for cancer immunotherapy is also discussed. Ganglioside Structures and BiosynthesisGangliosides are acidic GSL containing from one to five sialic acids residues. They are mainly, but not exclusively, derived from ganglio-series GSL (GgCer) that result from the substitution of a ceramide (Cer) by the tetrasaccharide core Galβ1-3GalNAcβ1-4Galβ1-4Glcβ (Gg4). In different cell types and tissues, gangliosides are usually found as a mixture of di-, tri-and tetrasaccharide cores substituted by one or more sialic acid residues [1,5]. The biosynthesis of gangliosides takes place in the Golgi apparatus and starts by the transfer of sialic acid residues to lactosylceramide (LacCer) by specific sialyltransferases, i.e., the CMP-Neu5Ac: LacCer α2,3-sialyltransferase ST3Gal V (GM3 synthase) [6], the CMP-Neu5Ac: GM3 α2,8-sialyltransferase ST8Sia I (GD3 synthase) [7] and the CMP-Neu5Ac: GD3 α2,8-sialyltransferase ST8Sia V [8], that show high specificity toward glycolipid substrates [9]. Thus, LacCer, GM3, GD3 and GT3 are the precursors for 0-, a-, b-and c-series gangliosides, respectively (Figure 1).

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Estradiol Represses the GD3 Synthase Gene ST8SIA1 Expression in Human Breast Cancer Cells by Preventing NFκB Binding to ST8SIA1 Promoter

Cited by 32 publications

References 52 publications

Role of Cytokine-Induced Glycosylation Changes in Regulating Cell Interactions and Cell Signaling in Inflammatory Diseases and Cancer

Role of Cytokine-Induced Glycosylation Changes in Regulating Cell Interactions and Cell Signaling in Inflammatory Diseases and Cancer

Selectin Ligands Sialyl-Lewis a and Sialyl-Lewis x in Gastrointestinal Cancers

O-acetylated Gangliosides as Targets for Cancer Immunotherapy

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