RNAseq of ST6GAL1-wild type and ST6GAL1-knock out cells of MDA-MB-231 cells.
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE174080 | GEO | 2022/12/01
REPOSITORIES: GEO
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Project description:Sialic acids on vertebrate cell surfaces mediate many biological roles. Altered expression of certain sialic acid types or their linkages can have prognostic significance in human cancer. A classic but unexplained example is enhanced α2-6-sialylation on N-glycans, resulting from over-expression of the Golgi enzyme β-galactoside:α2-6-sialyltransferase (ST6Gal-I). Previous data supporting a role for the resulting Siaα2-3Galβ1-4GlcNAc (Sia6LacNAc) structure in tumor biology were based on in vitro studies in transfected carcinoma cells, in which increased Sia6LacNAc on β1-integrins enhanced their binding to ligands, and stimulated cell motility. Here we examine for the first time the in vivo role of the ST6Gal-I enzyme in the growth and differentiation of spontaneous mammary cancers in mice transgenic for an MMTV-promoter-driven polyoma-middle-T antigen, a tumor in which beta1-integrin function is important for tumorigenesis, and in maintaining the proliferative state of tumor cells. Tumors induced in St6gal1 null animals were more differentiated in comparison to those in the wild-type background, both by histological analysis and by protein expression profiles. Furthermore, we show the St6gal1 null tumors have selectively altered expression of genes associated with focal adhesion signaling, and have decreased phosphorylation of FAK, a downstream target of β1-integrins. This first in vivo evidence for a role of ST6Gal-I in tumor progression was confirmed using a novel approach, which conditionally restored St6gal1 in cell lines derived from the null tumors. These findings indicate a role for ST6Gal-I as a mediator of tumor progression, with its expression causing a less differentiated phenotype, via enhanced β1-integrin function. Experiment Overall Design: Messenger RNA from tumors arising in wild-type or St6gal1 null littermates was used for the gene expression analysis on the Mouse Genome 430 2.0 Array (Affymetrix). Six PyV-mT St6gal1 null and wild-type tumor pairs were used, in four independent pools of three tumors each. Each sample is a pool of three different tumors from three different animals. For the first set of microarray analysis samples GSM239969 and GSM239970 were being compared, and in the second set, samples GSM239971 and GSM239972 were compared.
2008-06-16 | E-GEOD-9447 | biostudies-arrayexpress
Project description:This study describes a novel function for the ST6GAL1 sialyltransferase in promoting acinar to ductal metaplasia (ADM). ST6GAL1 activity facilitates ADM by reprogramming acinar cells into a more progenitor-like state.
2023-09-05 | GSE234045 | GEO
Project description:Normal early human B-cells development from lymphoid progenitors in the bone marrow is dependent upon instructions from elements in that microenvironment which include stromal cells as well as extracellular matrix and factors secreted by these cells. Glycosylation is thought to play a key role in such interactions. The sialyltransferase ST6Gal1, with high expression in specific hematopoietic cell types, is the only enzyme thought to catalyze the terminal addition of sialic acids in an a2-6-linkage to galactose on N-glycans in such cells. Expression of ST6Gal1 increases as mouse B cells undergo normal B-lineage differentiation. B-cell precursor acute lymphoblastic leukemias (BCP-ALL) with differentiation arrest at various stages of early B-cell development have widely different expression levels of ST6GALl1 at diagnosis, with high ST6Gal1 in some relapses. We analyzed the consequences of increased ST6Gal1 expression in a diagnosis sample using lentiviral transduction of ST6Gal1 into US7 cells which have a relatively low level of ST6Gal1 expression. Controls were transduced with an empty vector. Gene expression analysis using RNA-seq showed a surprisingly large number of genes with significant differential expression, of which around 60% showed increased transcript levels, in the ST6Gal1 overexpressing BCP-ALL cells.
2022-04-06 | GSE185611 | GEO
Project description:Rattus norvegicus St6gal1, ST6 beta-galactoside alpha-2,6-sialyltransferase 1 [Source:RGD Symbol;Acc:3676], is expressed in 4 baseline experiment(s);
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Project description:Mus musculus St6gal1, beta galactoside alpha 2,6 sialyltransferase 1 [Source:MGI Symbol;Acc:MGI:108470], is differentially expressed in 151 experiment(s);
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Project description:Rattus norvegicus St6gal1, ST6 beta-galactoside alpha-2,6-sialyltransferase 1 [Source:RGD Symbol;Acc:3676], is differentially expressed in 36 experiment(s);
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Project description:Monodelphis domestica ST6GAL1, ST6 beta-galactoside alpha-2,6-sialyltransferase 1 [Source:NCBI gene;Acc:100617174], is expressed in 2 baseline experiment(s);
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Project description:Mus musculus St6gal1, beta galactoside alpha 2,6 sialyltransferase 1 [Source:MGI Symbol;Acc:MGI:108470], is expressed in 37 baseline experiment(s);
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Project description:The clinical performance of trastuzumab in the treatment of ErbB2-positive gastric cancer is severely hampered by the emergence of molecular resistance. The glycosylation landscape of ErbB2’s extracellular domain, and the molecular mechanisms through which it tunes gastric cell malignancy, including the acquisition of trastuzumab resistance, remain elusive. We show that the expression of ErbB2 sialylated glycoforms holds clinical utility in the prediction of clinical outcome and stratification of gastric cancer patients. In-depth glycoproteomic and glycomic analysis of ErbB2 extracellular region disclosed a site-specific profile in gastric cancer cells. We further demonstrate that ST6Gal1 sialyltransferase specifically targets ErbB2 N-glycosylation sites within the trastuzumab binding domain. Moreover, the abrogation of ST6Gal1-mediated α2,6-sialylation reshapes ErbB2 glycome and sensitizes gastric cancer cells to trastuzumab-induced cytotoxicity through receptor membrane stabilization and a downregulation of ErbB2 activation. Overall, this data demonstrates that aberrant sialylation tunes the molecular resistance of ErbB2-driven gastric cancer cells to trastuzumab.
2021-05-11 | PXD017609 | Pride
Project description:Sus scrofa ST6GAL1, ST6 beta-galactoside alpha-2,6-sialyltransferase 1 [Source:VGNC Symbol;Acc:VGNC:93507], is differentially expressed in 3 experiment(s);
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