ArticlePloS one2011
The recognition of N-glycans by the lectin ArtinM mediates cell death of a human myeloid leukemia cell line.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 39 citations in OpenAlex.
- From inflammation to immune regulation: The dual nature of dietary lectins in health and disease.Heliyon · 2024Review
- ArtinM Cytotoxicity in B Cells Derived from Non-Hodgkin's Lymphoma Depends on Syk and Src Family Kinases.International journal of molecular sciences · 2023Article
- Targeting Drug Chemo-Resistance in Cancer Using Natural Products.Biomedicines · 2021Review
- MytiLec-1 Shows Glycan-Dependent Toxicity against Brine ShrimpMarine drugs · 2019Article
- The Response of IL-17-Producing B Cells to ArtinM Is Independent of Its Interaction with TLR2 and CD14.Molecules (Basel, Switzerland) · 2018Article
- CD14 is critical for TLR2-mediated M1 macrophage activation triggered by N-glycan recognition.Scientific reports · 2017Article
- ArtinM Mediates Murine T Cell Activation and Induces Cell Death in Jurkat Human Leukemic T Cells.International journal of molecular sciences · 2017Article
- Natural Compounds As Modulators of Non-apoptotic Cell Death in Cancer Cells.Current genomics · 2017Article
- Lectins, Interconnecting Proteins with Biotechnological/Pharmacological and Therapeutic Applications.Evidence-based complementary and alternative medicine : eCAM · 2017Review
- Radiosensitisation of human glioma cells by inhibition of β1,6-GlcNAc branched N-glycans.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Evaluating the Equilibrium Association Constant between ArtinM Lectin and Myeloid Leukemia Cells by Impedimetric and Piezoelectric Label Free Approaches.Biosensors · 2014Article
- A lectin with highly potent inhibitory activity toward breast cancer cells from edible tubers of Dioscorea opposita cv. nagaimo.PloS one · 2013Article
- Detection of glycomic alterations induced by overexpression of p-glycoprotein on the surfaces of L1210 cells using sialic acid binding lectins.International journal of molecular sciences · 2012Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ArtinM, a D-mannose-binding lectin from Artocarpus heterophyllus (jackfruit), interacts with N-glycosylated receptors on the surface of several cells of hematopoietic origin, triggering cell migration, degranulation, and cytokine release. Because malignant transformation is often associated with altered expression of cell surface glycans, we evaluated the interaction of ArtinM with human myelocytic leukemia cells and investigated cellular responses to lectin binding. The intensity of ArtinM binding varied across 3 leukemia cell lines: NB4>K562>U937. The binding, which was directly related to cell growth suppression, was inhibited in the presence of Manα1-3(Manα1-6)Manβ1, and was reverted in underglycosylated NB4 cells. ArtinM interaction with NB4 cells induced cell death (IC(50) = 10 µg/mL), as indicated by cell surface exposure of phosphatidylserine and disruption of mitochondrial membrane potential unassociated with caspase activation or DNA fragmentation. Moreover, ArtinM treatment of NB4 cells strongly induced reactive oxygen species generation and autophagy, as indicated by the detection of acidic vesicular organelles in the treated cells. NB4 cell death was attributed to ArtinM recognition of the trimannosyl core of N-glycans containing a ß1,6-GlcNAc branch linked to α1,6-mannose. This modification correlated with higher levels of N-acetylglucosaminyltransferase V transcripts in NB4 cells than in K562 or U937 cells. Our results provide new insights into the potential of N-glycans containing a β1,6-GlcNAc branch linked to α1,6-mannose as a novel target for anti-leukemia treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.