ArticleOncotarget2016
An increase in galectin-3 causes cellular unresponsiveness to IFN-γ-induced signal transduction and growth inhibition in gastric cancer cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The trial behind it
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- EGFR: New Insights on Its Activation and Mutation in Tumor and Tumor Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- A Narrative Review on the Multifaceted Roles of Galectins in Host-Pathogen Interactions DuringInternational journal of molecular sciences · 2025Review
- Review
- Early Cardiac Ischemia-Reperfusion Injury: Interactions of Autophagy with Galectin-3 and Oxidative Stress.Biomedicines · 2024Article
- Targeting galectin-driven regulatory circuits in cancer and fibrosis.Nature reviews. Drug discovery · 2023Review
- Immunomodulation exerted by galectins: a land of opportunity in rare cancers.Frontiers in immunology · 2023Review
- Antitumour immunity regulated by aberrant ERBB family signalling.Nature reviews. Cancer · 2021Review
- MiR-424-3p suppresses galectin-3 expression and sensitizes ovarian cancer cells to cisplatin.Archives of gynecology and obstetrics · 2019Article
- Morin decreases galectin-3 expression and sensitizes ovarian cancer cells to cisplatin.Archives of gynecology and obstetrics · 2018Article
- Galectin-3 deficiency drives lupus-like disease by promoting spontaneous germinal centers formation via IFN-γ.Nature communications · 2018Article
- Role of Galectins in Tumors and in Clinical Immunotherapy.International journal of molecular sciences · 2018Review
- Escape from IFN-γ-dependent immunosurveillance in tumorigenesis.Journal of biomedical science · 2017Review
- The Many Roles of Galectin-3, a Multifaceted Molecule, in Innate Immune Responses against Pathogens.Mediators of inflammation · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glycogen synthase kinase (GSK)-3β facilitates interferon (IFN)-γ signaling by inhibiting Src homology-2 domain-containing phosphatase (SHP) 2. Mutated phosphoinositide 3-kinase (PI3K) and phosphatase and tensin homolog (PTEN) cause AKT activation and GSK-3β inactivation to induce SHP2-activated cellular unresponsiveness to IFN-γ in human gastric cancer AGS cells. This study investigated the potential role of galectin-3, which acts upstream of AKT/GSK-3β/SHP2, in gastric cancer cells. Increasing or decreasing galectin-3 altered IFN-γ signaling. Following cisplatin-induced galectin-3 upregulation, surviving cells showed cellular unresponsiveness to IFN-γ. Galectin-3 induced IFN-γ resistance independent of its extracellular β-galactoside-binding activity. Galectin-3 expression was not regulated by PI3K activation or by a decrease in PTEN. Increased galectin-3 may cause GSK-3β inactivation and SHP2 activation by promoting PDK1-induced AKT phosphorylation at a threonine residue. Overexpression of AKT, inactive GSK-3βR96A, SHP2, or active SHP2D61A caused cellular unresponsiveness to IFN-γ in IFN-γ-sensitive MKN45 cells. IFN-γ-induced growth inhibition and apoptosis in AGS cells were observed until galectin-3 expression was downregulated. These results demonstrate that an increase in galectin-3 facilitates AKT/GSK-3β/SHP2 signaling, causing cellular unresponsiveness to IFN-γ.
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Registered trials
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.