ArticleWorld journal of biological chemistry2011
Galectin-1-mediated biochemical controls of melanoma and glioma aggressive behavior.
Article in World journal of biological chemistry, 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, 29 citations in OpenAlex.
- Glycobiology-driven therapeutic targeting of glycan-binding proteins: mechanisms, diseases, and clinical translation.Signal transduction and targeted therapy · 2026Review
- The role of galectins in modulating the tumor microenvironment and driving metastasis in skin cancers.Biological research · 2026Review
- Knockdown of the Shwachman-Diamond syndrome gene, SBDS, induces galectin-1 expression and impairs cell growth.International journal of hematology · 2024Article
- Autocrine Signaling of NRP1 Ligand Galectin-1 Elicits Resistance to BRAF-Targeted Therapy in Melanoma Cells.Cancers · 2020Article
- Galectin-1 gene silencing inhibits the activation and proliferation but induces the apoptosis of hepatic stellate cells from mice with liver fibrosis.International journal of molecular medicine · 2019Article
- Galectin-1 Inhibitor OTX008 Induces Tumor Vessel Normalization and Tumor Growth Inhibition in Human Head and Neck Squamous Cell Carcinoma Models.International journal of molecular sciences · 2017Article
- Sensitization of glioblastoma tumor micro-environment to chemo- and immunotherapy by Galectin-1 intranasal knock-down strategy.Scientific reports · 2017Article
- Melanoma and the Unfolded Protein Response.Cancers · 2016Review
- Galectins in cancer: carcinogenesis, diagnosis and therapy.Annals of translational medicine · 2014Review
- Hierarchical and selective roles of galectins in hepatocarcinogenesis, liver fibrosis and inflammation of hepatocellular carcinoma.World journal of gastroenterology · 2013Review
- The clinical implication of tumoral Gal-1 expression in laryngeal squamous cell carcinomas.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2013Article
- Structure-based optimization of angiostatic agent 6DBF7, an allosteric antagonist of galectin-1.The Journal of pharmacology and experimental therapeutics · 2013Article
- Induction of the unfolded protein response drives enhanced metabolism and chemoresistance in glioma cells.PloS one · 2013Article
- Galectin-1 as an oncotarget in gliomas and melanomas.Oncotarget · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gliomas and melanomas are associated with dismal prognosis because of their marked intrinsic resistance to proapoptotic stimuli, such as conventional chemotherapy and radiotherapy, as well as their ability to escape immune cell attacks. In addition, gliomas and melanomas display pronounced neoangiogenesis. Galectin-1 is a hypoxia-sensitive protein, which is abundantly secreted by glioma and melanoma cells, which displays marked proangiogenic effects. It also provides immune tolerogenic environments to melanoma and glioma cells through the killing of activated T cells that attack these tumor cells. Galectin-1 protects glioma and melanoma cells against cytotoxic insults (including chemotherapy and radiotherapy) through a direct role in the unfolded protein response. Altogether, these facts clearly point to galectin-1 as an important target to be combated in gliomas and melanomas in order to: (1) weaken the defenses of these two types of cancers against radiotherapy, chemotherapy and immunotherapy/vaccine therapy; and (2) reinforce antiangiogenic therapies. In the present article, we review the biochemical and molecular biology-related pathways controlled by galectin-1, which are actually beneficial for melanoma and glioma cells, and therefore detrimental for melanoma and glioma patients.
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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.