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ST3GAL1-Associated Transcriptomic Program in Glioblastoma Tumor Growth, Invasion, and Prognosis

ABSTRACT: Cell surface sialylation confers many roles in cancer biology including cell proliferation, invasiveness, metastasis and angiogenesis. We show here that ST3Gal1 sialyltransferase marks a self-renewing cellular fraction. Depletion of ST3GAL1 abrogates glioma cell growth and tumorigenicity. In contrast, TGFb induces ST3GAL1 expression and correlates with the pattern of ST3Gal1 activation in patient tumors of the mesenchymal molecular subtype. To delineate the downstream events of ST3Gal1 signaling, we utilized a bioinformatical approach that leveraged on the greater statistical power of large patient databases, and subsequently verified our predictions in patient-derived glioma cells. We identify FoxM1, a major stem cell regulatory gene, as a downstream effector, and show that ST3Gal1 mediates the glioma phenotype through control of FoxM1 protein degradation

ORGANISM(S): Homo sapiens

PROVIDER: GSE51411 | GEO | 2015/11/09

SECONDARY ACCESSION(S): PRJNA222988

REPOSITORIES: GEO

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ST3GAL1-Associated Transcriptomic Program in Glioblastoma Tumor Growth, Invasion, and Prognosis

Project description:Cell surface sialylation confers many roles in cancer biology including cell proliferation, invasiveness, metastasis and angiogenesis. We show here that ST3Gal1 sialyltransferase marks a self-renewing cellular fraction. Depletion of ST3GAL1 abrogates glioma cell growth and tumorigenicity. In contrast, TGFb induces ST3GAL1 expression and correlates with the pattern of ST3Gal1 activation in patient tumors of the mesenchymal molecular subtype. To delineate the downstream events of ST3Gal1 signaling, we utilized a bioinformatical approach that leveraged on the greater statistical power of large patient databases, and subsequently verified our predictions in patient-derived glioma cells. We identify FoxM1, a major stem cell regulatory gene, as a downstream effector, and show that ST3Gal1 mediates the glioma phenotype through control of FoxM1 protein degradation Total RNA from primary neurosphere culture of brain tumor specimens non-treated and ST3GAL1 KD clones. The mRNAs of 5 unique glioma propagating cells (GPCs) were hybridized on Affymetrix HG-U133 Plus2 chips to study the transcriptomic impact of ST3GAL1 knock-down. Specimens were obtained from 5 glioma patients and replicate arrays were performed for all 5 neurosphere cultures.

2015-11-09 | E-GEOD-51395 | biostudies-arrayexpress

ST3GAL1-Associated Transcriptomic Program in Glioblastoma Tumor Growth, Invasion, and Prognosis

2015-11-09 | GSE51395 | GEO

ST3GAL1-Associated Transcriptomic Program in Glioblastoma Tumor Growth, Invasion, and Prognosis

Project description:Cell surface sialylation confers many roles in cancer biology including cell proliferation, invasiveness, metastasis and angiogenesis. We show here that ST3Gal1 sialyltransferase marks a self-renewing cellular fraction. Depletion of ST3GAL1 abrogates glioma cell growth and tumorigenicity. In contrast, TGFb induces ST3GAL1 expression and correlates with the pattern of ST3Gal1 activation in patient tumors of the mesenchymal molecular subtype. To delineate the downstream events of ST3Gal1 signaling, we utilized a bioinformatical approach that leveraged on the greater statistical power of large patient databases, and subsequently verified our predictions in patient-derived glioma cells. We identify FoxM1, a major stem cell regulatory gene, as a downstream effector, and show that ST3Gal1 mediates the glioma phenotype through control of FoxM1 protein degradation Total RNA from primary neurosphere culture of brain tumor specimens were flow-sorted to identify Peanut Agglutinin(PNA) affinity. The fractions of different degress of PNA bound GPCs were hybridized on Illumina Human Ref-8v2 bead chips to study the impact of transcriptome pattern of PNA affinity. Specimens were obtained from 4 patients and replicate arrays were performed for all 4 neurosphere cultures.

2015-11-09 | E-GEOD-51411 | biostudies-arrayexpress

St3gal1 and bII-spectrin pathways control CAR-T cell migration to target tumor sites [2]

Project description:Adoptive transfer of genetically engineered chimeric antigen receptor (CAR)-T cell is emerging as a promising treatment option for hematological malignancies. However, T cell immunotherapies have largely failed in patients with solid tumors. Here, with a CRISPR-Cas9 pooled library, we performed an in vivo targeted loss-of-function screen and identified ST3 b-galactoside a-2,3-sialyltransferase 1 (St3gal1) as a key negative regulator of the cancer-specific migration of CAR-T cells. Analysis of glycosylated proteins reveals that CD18 is a major effector of St3gal1 in activated CD8 T cells. St3gal1-mediated glycosylation induces the spontaneous nonspecific tissue sequestration of T cells by altering lymphocyte function-associated antigen-1 (LFA-1) endocytic recycling. Engineered CAR-T cells with enhanced expression of bII-spectrin, a key LFA-1 associated cytoskeleton molecule, reversed St3gal1-mediated nonspecific T cell migration and significantly reduced tumor growth in mice by improving tumor-specific homing of CAR-T cells. These findings identify a role of the St3gal1- bII-spectrin axis as the key cell-intrinsic program for cancer targeting CAR-T cell migration and as a promising strategy for effective T cell immunotherapy.

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St3gal1 and bII-spectrin pathways control CAR-T cell migration to target tumor sites [1]

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St3gal1 and bII-spectrin pathways control CAR-T cell migration to target tumor sites [3]

2023-03-17 | GSE227509 | GEO

RNAseq of ST6GAL1-wild type and ST6GAL1-knock out cells of MDA-MB-231 cells.

Project description:Dynamic change of glycosylation is found in various cancers; however, the precise role of glycosylation in metastasis is remained largely unknown. Current study show that α2,6-sialylation or β-galactoside α2,6-sialyltransferase (ST6Gal1) inhibits circulating tumor cell aggregation and depletion or restoration of α2,6-sialylation in patient derived xenograft model amplified or diminished cell aggregation and lung metastasis.

2022-12-01 | GSE174080 | GEO

Inherited defect in ST6GalNAc1 reveals roles of sialylation in intestinal homeostasis

Project description:Chronic inflammatory bowel disease (IBD) causes disability, suffering and risk of colon cancer in over 30 million people globally. Here, we investigate 3 kindreds of IBD with mutations in the N-acetylgalactosamide alpha-2,6-sialyltransferase 1/ST6GALNAC1 (ST6) glycosyltransferase gene that is uniquely expressed in the goblet cells (GCs). These mutations cause defective sialic acid (SA) conjugation, elimination of the onco-antigen S-Tn (Sialyl-Tn), and altered glycosylation of the MUC2 protein, a key component of intestinal mucus. Decreased MUC2 sialylation increases susceptibility to bacterial proteolytic degradation and compromises the gastrointestinal (GI) mucus barrier. Mice harboring the patient ST6 mutations recapitulate human colitis and reveal that defective sialylation causes dysbiosis, butyrate overproduction, and impaired GI stem cell proliferation during injury. Thus, this new genetic disease illustrates how sialylation controls host-microbe homeostasis and reveals several new potential approaches to IBD treatment.

2022-03-16 | GSE183821 | GEO

Inherited defect in ST6GalNAc1 reveals roles of sialylation in intestinal homeostasis

2022-03-17 | PXD028239 | Pride

Targeting stromal cell sialylation reverses T cell mediated immunosuppression in the tumor microenvironment

Project description:Immunosuppressive tumor microenvironments (TME) reduce the effectiveness of immune responses in cancer. Mesenchymal stromal cells (MSC), precursors to cancer-associated fibroblasts (CAFs), dictate tumor progression by enhancing immune cell suppression in colorectal cancer (CRC). Hyper-sialylation of glycans promotes immune evasion in cancer through binding of sialic acids to their receptors, Siglecs, expressed on immune cells that results in inhibition of effector functions. The role of sialylation in dictating MSC/CAF immunosuppression in the TME is unknown. In this study, we show that tumor-conditioned stromal cells have increased sialyltransferase expression, α2,3/6-linked sialic acid and Siglec ligands. Tumor-conditioned stromal cells and CAFs induce exhausted immunomodulatory PD-1, Siglec-7 and Siglec-9-expressing T cell phenotypes. In vivo, targeting stromal cell sialylation reverses stromal cell-mediated immunosuppression, as evidenced by infiltration of CD25 and granzyme B-expressing T cells in the tumor and draining lymph node. Targeting stromal cell sialylation may overcome immunosuppression in the CRC TME.

2023-05-22 | GSE229054 | GEO

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