ArticleProceedings of the National Academy of Sciences of the United States of America2022
Antibody-mediated blockade for galectin-3 binding protein in tumor secretome abrogates PDAC metastasis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 18 citations in OpenAlex.
- S100A4 promotes collective invasion of pancreatic ductal adenocarcinoma and its blockade suppresses metastasis.Cell communication and signaling : CCS · 2026Article
- Expression, Localization and Actions of Galectin-3: Implications in the Pathophysiology and Therapy of Cardiovascular Disease.International journal of molecular sciences · 2026Review
- Exosome-mediated miR-4660 delivery inhibits OPN promoted hepatoma cells aggression through targeting LGALS3BP.Journal of cell communication and signaling · 2026Article
- Galectin-3 Binds to the Allosteric Site and Activates Integrins αvβ3, αIIbβ3, and α5β1, and Lactose Inhibits This Activation.Biomolecules · 2026Article
- The Galectin-3-binding protein promotes angiogenesis in pancreatic cancer via simultaneous upregulation of VEGFA and direct HUVEC activation mediated by and VAMP5-STAT3.Cell communication and signaling : CCS · 2026Article
- Glycosylated LGALS3BP is highly secreted by bladder cancer cells and represents a novel urinary disease biomarker.Molecular oncology · 2026Article
- Comprehensive prognostic and immune infiltration assessment of LGALS3BP in pan-cancer patients.Discover oncology · 2026Article
- Galectin-3 binds to the RGD-binding site in a glycan-independent manner and to the allosteric site and activates integrins αvβ3, αIIbβ3, and α5β1.bioRxiv : the preprint server for biology · 2026Article
- Galectin-3 promotes FBXL5-dependent ubiquitination and degradation of YAP1 to constrain colorectal cancer growth.Frontiers in immunology · 2026Article
- Galectins at the crossroads of tumor immunity, metabolism, and metastasis: mechanisms, therapeutic resistance, and translational opportunities.Frontiers in immunology · 2026Review
- LGALS3BP antibody-drug conjugate enhances tumor-infiltrating lymphocytes and synergizes with immunotherapy to restrain neuroblastoma growth.Journal of translational medicine · 2025Article
- Secreted LGALS3BP facilitates distant metastasis of breast cancer.Breast cancer research : BCR · 2025Article
- Tumor-associated Tn and STn antigens: from molecular mechanism to precision diagnosis and treatment.Frontiers in immunology · 2025Review
- The supporting role of Schwann cells in perineural invasion of pancreatic ductal adenocarcinoma.Frontiers in pharmacology · 2025Review
- Is Immunohistochemical Galectin-3 Expression Associated with the Epithelial-Mesenchymal Transition in High- and Low-Grade Invasive Urothelial Carcinomas of the Bladder?Diagnostics (Basel, Switzerland) · 2024Article
- Clinical Significance of Abnormal Serum LGALS3BP Expression in Patients with Idiopathic Inflammatory Myopathies.Journal of inflammation research · 2024Article
- Galectin-3's Complex Interactions in Pancreatic Ductal Adenocarcinoma: From Cellular Signaling to Therapeutic Potential.Biomolecules · 2023Review
- Functional and Clinical Proteomic Exploration of Pancreatic Cancer.Molecular & cellular proteomics : MCP · 2023Review
- Galectins dysregulation: A way for cancer cells to invade and pervade.Oncology research · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 2 institutions in 1 country.
Funding
Abstract
The major challenges in pancreatic ductal adenocarcinoma (PDAC) management are local or distant metastasis and limited targeted therapeutics to prevent it. To identify a druggable target in tumor secretome and to explore its therapeutic intervention, we performed a liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based proteomic analysis of tumors obtained from a patient-derived xenograft model of PDAC. Galectin-3 binding protein (Gal-3BP) is identified as a highly secreted protein, and its overexpression is further validated in multiple PDAC tumors and primary cells. Knockdown and exogenous treatment of Gal-3BP showed that it is required for PDAC cell proliferation, migration, and invasion. Mechanistically, we revealed that Gal-3BP enhances galectin-3-mediated epidermal growth factor receptor signaling, leading to increased cMyc and epithelial-mesenchymal transition. To explore the clinical impact of these findings, two antibody clones were developed, and they profoundly abrogated the metastasis of PDAC cells in vivo. Altogether, our data demonstrate that Gal-3BP is an important therapeutic target in PDAC, and we propose its blockade by antibody as a therapeutic option for suppressing PDAC metastasis.
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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.