glycan/hypoxie

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Linking tumor hypoxia with VEGFR2 signaling and compensatory angiogenesis: Glycans make the difference.

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Although blocking vascular endothelial growth factor (VEGF) signaling is clinically beneficial in certain cancers, tumor regrowth in treated patients suggests that compensatory angiogenic programs may limit the efficacy of anti-VEGF treatment. We found that association of galectin-1 with complex

Hypoxia and serum deprivation induces glycan alterations in triple negative breast cancer cells.

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Triple negative breast cancer (TNBC) is a major global public health problem. The lack of targeted therapy and the elevated mortality evidence the need for better knowledge of the tumor biology. Hypoxia and aberrant glycosylation are associated with advanced stages of malignancy, tumor progression

Hypoxia inducible factor 1α down regulates cell surface expression of α1,2-fucosylated glycans in human pancreatic adenocarcinoma cells.

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The α1,2-fucosyltransferase activity in pancreatic tumors is much lower compared to normal pancreatic tissue. Here we show that hypoxia inducible factor (HIF) 1α is constitutively expressed in the pancreatic cancer cell lines Pa-Tu-8988S and Pa-Tu-8988T and suppresses the expression of the

Regulatory role of glycans in the control of hypoxia-driven angiogenesis and sensitivity to anti-angiogenic treatment.

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Abnormal glycosylation is a typical hallmark of the transition from healthy to neoplastic tissues. Although the importance of glycans and glycan-binding proteins in cancer-related processes such as tumor cell adhesion, migration, metastasis and immune escape has been largely appreciated, our

Altered expression of glycan genes in cancers induced by epigenetic silencing and tumor hypoxia: clues in the ongoing search for new tumor markers.

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The glycan molecules that preferentially appear in cancers are clinically utilized as serum tumor markers. The exact reason, however, why glycans are useful as tumor markers remain elusive. Here, we will summarize lessons learned from well-established cancer-associated glycans, and propose

Glycobiology Modifications in Intratumoral Hypoxia: The Breathless Side of Glycans Interaction.

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Post-translational and co-translational enzymatic addition of glycans (glycosylation) to proteins, lipids, and other carbohydrates, is a powerful regulator of the molecular machinery involved in cell cycle, adhesion, invasion, and signal transduction, and is usually seen in both in vivo and in vitro

Disrupting galectin-1 interactions with N-glycans suppresses hypoxia-driven angiogenesis and tumorigenesis in Kaposi's sarcoma.

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Kaposi's sarcoma (KS), a multifocal vascular neoplasm linked to human herpesvirus-8 (HHV-8/KS-associated herpesvirus [KSHV]) infection, is the most common AIDS-associated malignancy. Clinical management of KS has proven to be challenging because of its prevalence in immunosuppressed patients and its

The chemistry of negotiation: rhythmic, glycan-driven acidification in a symbiotic conversation.

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Glycans have emerged as critical determinants of immune maturation, microbial nutrition, and host health in diverse symbioses. In this study, we asked how cyclic delivery of a single host-derived glycan contributes to the dynamic stability of the mutualism between the squid Euprymna scolopes and its

Altered sphingolipid metabolism induced by tumor hypoxia - new vistas in glycolipid tumor markers.

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Uncontrolled growth of malignant cells produces hypoxic regions in locally advanced tumors. Recently we showed that tumor hypoxia-induced transcription of multiple genes involved in glycan synthesis, leading to expression of useful glycolipid tumor markers, such as gangliosides having N-glycolyl

Bisecting N-Acetylglucosamine Structures Inhibit Hypoxia-Induced Epithelial-Mesenchymal Transition in Breast Cancer Cells.

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The epithelial-mesenchymal transition (EMT) process plays a key role in many biological processes, including tissue fibrosis, metastatic diseases, and cancer progression. EMT can be induced by certain factors, notably hypoxia, in the tumor microenvironment. Aberrant levels of certain N-glycans is

Fluorescent Detection of O-GlcNAc via Tandem Glycan Labeling

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O-GlcNAcylation is a reversible serine/threonine glycosylation on cytosolic and nuclear proteins that are involved in various regulatory pathways. However, the detection and quantification of O-GlcNAcylation substrates have been challenging. Here, we report a highly efficient method

Altered susceptibility to apoptosis and N‑glycan profiles of hematopoietic KG1a cells following co‑culture with bone marrow‑derived stromal cells under hypoxic conditions.

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Mesenchymal stromal cells are an important component of the bone marrow microenvironment (niche), where they support hematopoiesis via direct cell‑cell interactions with hematopoietic stem and progenitor cells, and by releasing soluble factors. Glycans, including N‑glycans, are involved in numerous

Hypoxia enhances the malignant nature of bladder cancer cells and concomitantly antagonizes protein O-glycosylation extension.

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Invasive bladder tumours express the cell-surface Sialyl-Tn (STn) antigen, which stems from a premature stop in protein O-glycosylation. The STn antigen favours invasion, immune escape, and possibly chemotherapy resistance, making it attractive for target therapeutics. However, the events leading to

Expression of fucosylated glycans in endothelial glycocalyces of placental villi at early and late fetal growth restriction.

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The aim of the study was to investigate the content and distribution of fucosylated sugar residues and Lewis Y (Le^Y) in the endothelial glycocalyx (eGC) in placental tissue at early and late onset fetal growth restriction (FGR). Our findings demonstrated that the changes of the

Hypoxia Alters Epigenetic and N-Glycosylation Profiles of Ovarian and Breast Cancer Cell Lines in-vitro

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Background: Glycosylation is one of the most fundamental post-translational modifications. Importantly, glycosylation is altered in many cancers. These alterations have been proven to impact on tumor progression and to promote tumor cell survival. From the literature, it is known that there

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