ArticleJournal of cellular and molecular medicine2014
Altered β1,6-GlcNAc branched N-glycans impair TGF-β-mediated epithelial-to-mesenchymal transition through Smad signalling pathway in human lung cancer.
Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Pooled it
- Transcriptome combined with single-cell data to construct a prognostic model for glycosylation-related genes in osteosarcoma.Discover oncology · 2026Article
- Differential AXL expression and Arf1 regulation control stiffness-dependent Golgi organization in breast cancer cells.Journal of cell science · 2026Article
- Down-regulation of MFNG promotes the metastatic potential of lung adenocarcinoma by regulating TGF-β/Smad signaling.iScience · 2025Article
- Glycosylation in T2 high and Th17 Asthma: A Narrative Review.Journal of asthma and allergy · 2025Review
- Exploration of glycosyltransferases mutation status in cervical cancer reveals PARP14 as a potential prognostic marker.Glycoconjugate journal · 2023Article
- Aberrant N-glycosylation in cancer: MGAT5 and β1,6-GlcNAc branched N-glycans as critical regulators of tumor development and progression.Cellular oncology (Dordrecht, Netherlands) · 2023Review
- An integrated multi-omics approach to identify regulatory mechanisms in cancer metastatic processes.Genome biology · 2021Article
- Evidence That Tumor Microenvironment Initiates Epithelial-To-Mesenchymal Transition and Calebin A can Suppress it in Colorectal Cancer Cells.Frontiers in pharmacology · 2021Article
- Ursolic Acid Attenuates TGF-β1-Induced Epithelial-Mesenchymal Transition in NSCLC by Targeting Integrin αVβ5/MMPs Signaling.Oncology research · 2019Article
- TBL1XR1 as a potential therapeutic target that promotes epithelial-mesenchymal transition in lung squamous cell carcinoma.Experimental and therapeutic medicine · 2019Article
- N-glycosylation by N-acetylglucosaminyltransferase V enhances the interaction of CD147/basigin with integrin β1 and promotes HCC metastasis.The Journal of pathology · 2018Article
- The Function of Fucosylation in Progression of Lung Cancer.Frontiers in oncology · 2018Review
- Vasohibin 2 as a potential predictor of aggressive behavior of triple-negative breast cancer.American journal of translational research · 2017Article
- FAT4 functions as a tumor suppressor in triple-negative breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Silencing of Prrx1b suppresses cellular proliferation, migration, invasion and epithelial-mesenchymal transition in triple-negative breast cancer.Journal of cellular and molecular medicine · 2016Article
- The role of N-glycans in colorectal cancer progression: potential biomarkers and therapeutic applications.Oncotarget · 2016Review
- 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
- Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The change of oligosaccharide structure has been revealed to be crucial for glycoproteins' biological functions and cell biological characteristics. N-acetylglucosaminy transferase V (GnT-V), a key enzyme catalysing the reaction of adding β1, 6-N-acetylglucosamine (GlcNAc) on asparagine-linked oligosaccharides of cell proteins, has been implicated to a metastastic-promoting oncoprotein in some carcinomas. However, this correlation might not be subjected to all types of cancers, for example, in non-small cell lung cancers, low level of GnT-V expression is associated with relatively short survival time and poor prognosis. To explain the role of GnT-V in lung cancer progression, we studied the association of GnT-V expression with lung cancer EMT behaviour. We found that GnT-V expression was correlated with epithelial marker positively and mesenchymal marker negatively. GnT-V levels, as well as β1,6-GlcNAc branched N-glycans, were strongly reduced in TGF-β1-induced EMT of human lung adenocarcinoma A549 cells. Further studies showed that suppression of β1,6-GlcNAc branched N-glycans by inhibitor or GnT-V silencing in A549 cells could promote TGF-β1-induced EMT-like changes, cell migration and invasion. Meanwhile, overexpression of GnT-V impaired TGF-β1-induced EMT, migration and invasion. It suggests that GnT-V suppresses the EMT process of lung cancer cells through inhibiting the TGF-β/Smad signalling and its downstream transcription factors in a GnT-V catalytic activity-dependent manner. Taken together, the present study reveals a novel mechanism of GnT-V as a suppressor of both EMT and invasion in human lung cancer cells, which may be useful for fully understanding N-glycan's biological roles in lung cancer progression.
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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.