ArticleJournal of leukocyte biology2016
Galectin-12 inhibits granulocytic differentiation of human NB4 promyelocytic leukemia cells while promoting lipogenesis.
Article in Journal of leukocyte biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Glycobiology-driven therapeutic targeting of glycan-binding proteins: mechanisms, diseases, and clinical translation.Signal transduction and targeted therapy · 2026Review
- Multifaceted roles of Galectins: from carbohydrate binding to targeted cancer therapy.Biomarker research · 2025Review
- An Overview on Lipid Droplets Accumulation as Novel Target for Acute Myeloid Leukemia Therapy.Biomedicines · 2023Review
- Evaluation of Plasma Concentrations of Galectins-1, 2 and 12 in Psoriasis and Their Clinical Implications.Biomolecules · 2023Article
- The role of galectins in immunity and infection.Nature reviews. Immunology · 2023Review
- Galectin functions in cancer-associated inflammation and thrombosis.Frontiers in cardiovascular medicine · 2023Review
- Promoter methylation might shift the balance of Galectin-3 & 12 expression inFrontiers in genetics · 2023Article
- Galectins in Cancer and the Microenvironment: Functional Roles, Therapeutic Developments, and Perspectives.Biomedicines · 2021Review
- Lipid Droplets, the Central Hub Integrating Cell Metabolism and the Immune System.Frontiers in physiology · 2021Review
- Ablation of Galectin-12 Inhibits Atherosclerosis through Enhancement of M2 Macrophage Polarization.International journal of molecular sciences · 2020Article
- The Emerging Role of Galectins andCells · 2020Review
- Hypertriglyceridemia in Newly Diagnosed Acute Promyelocytic Leukemia.Frontiers in oncology · 2020Article
- PML-RARα interaction with TRIB3 impedes PPARγ/RXR function and triggers dyslipidemia in acute promyelocytic leukemia.Theranostics · 2020Article
- Galectin Targeted Therapy in Oncology: Current Knowledge and Perspectives.International journal of molecular sciences · 2018Review
- Galectin-12 in Cellular Differentiation, Apoptosis and Polarization.International journal of molecular sciences · 2018Review
Corrections and comments
- Commented on by
Authors and funding
4 authors at 2 institutions in 3 countries.
Funding
Abstract
As a member of the galectin family of animal lectins, galectin-12 is preferentially expressed in adipocytes and leukocytes. In adipocytes, galectin-12 is associated with lipid droplets and regulates lipid metabolism and energy balance, whereas its role in leukocytes is not clear. Analysis of galectin-12 expression in a public data set of acute myeloid leukemia (AML) samples revealed that it is selectively overexpressed in the M3 subtype, which is also known as acute promyelocytic leukemia (APL). To investigate the role of galectin-12 in APL cells, we manipulated its expression in the APL cell line, NB4, and measured resultant effects on all-trans-retinoic acid (ATRA)-induced granulocytic differentiation. With a doxycycline-inducible gene knockdown system, we found that suppression of galectin-12 promoted ATRA-induced neutrophil differentiation but inhibited lipid droplet formation. Our results indicate that overexpression of galectin-12 contributes to a differentiation block in APL cells, and suppression of galectin-12 facilitates granulocytic differentiation. Furthermore, these data suggest that lipogenesis and other aspects of myeloid differentiation can be differentially regulated. Taken together, these findings suggest that galectin-12 may be a target for treatment of the ATRA-resistant subset of APL.
Indexed as
Identifiers
What OpenQuestion holds
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.