ArticleCancers2020
Monocarboxylate Transporter 4 Regulates Glioblastoma Motility and Monocyte Binding Ability.
Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 20 citations in OpenAlex.
- Biotin-Decorated Inulin-Based Polymeric Micelles Unveil Their Dual-Targeting Ability for the Potential Treatment of Glioblastoma Multiforme through theMolecular pharmaceutics · 2026Article
- Selective regulation and cellular metabolism by the lactate transporter MCT4 in GBM.Medical oncology (Northwood, London, England) · 2025Article
- Exploring the role of monocarboxylate transporter 4 in diverse KRAS mutation subtypes of colorectal Cancer.Scientific reports · 2025Article
- The integrin adhesome and control of anti-tumour immunity.Biochemical Society transactions · 2024Review
- Metabolic Contrasts: Fatty Acid Oxidation and Ketone Bodies in Healthy Brains vs. Glioblastoma Multiforme.International journal of molecular sciences · 2024Review
- Inhibitory Effects of Urolithins, Bioactive Gut Metabolites from Natural Polyphenols, against Glioblastoma Progression.Nutrients · 2023Article
- Recent advances in label-free optical, electrochemical, and electronic biosensors for glioma biomarkers.Biomicrofluidics · 2023Review
- Prognostic value of lactate transporter SLC16A1 and SLC16A3 as oncoimmunological biomarkers associating tumor metabolism and immune evasion in glioma.Cancer innovation · 2022Article
- Anagliptin promotes apoptosis in mouse colon carcinoma cells via MCT-4/lactate-mediated intracellular acidosis.Experimental and therapeutic medicine · 2022Article
- Article
- Regulatory mechanism of HIF-1α and its role in liver diseases: a narrative review.Annals of translational medicine · 2022Review
- The role of SLC transporters for brain health and disease.Cellular and molecular life sciences : CMLS · 2021Review
- CHARTS: a web application for characterizing and comparing tumor subpopulations in publicly available single-cell RNA-seq data sets.BMC bioinformatics · 2021Article
- Comprehensive Analysis of the Relationship Between Metabolic Reprogramming and Immune Function in Prostate Cancer.OncoTargets and therapy · 2021Article
- CAIX Regulates GBM Motility and TAM Adhesion and Polarization through EGFR/STAT3 under Hypoxic Conditions.International journal of molecular sciences · 2020Article
- Glioblastoma Immune Landscape and the Potential of New Immunotherapies.Frontiers in immunology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is characterized by severe hypoxic and acidic stress in an abnormal microenvironment. Monocarboxylate transporter (MCT)4, a pH-regulating protein, plays an important role in pH homeostasis of the glycolytic metabolic pathways in cancer cells. The present study showed that GBM exposure to hypoxic conditions increased MCT4 expression. We further analyzed the glioma patient database and found that MCT4 was significantly overexpressed in patients with GBM, and the MCT4 levels positively correlated with the clinico-pathological grades of gliomas. We further found that MCT4 knockdown abolished the hypoxia-enhanced of GBM cell motility and monocyte adhesion. However, the overexpression of MCT4 promoted GBM cell migration and monocyte adhesion activity. Our results also revealed that MCT4-regulated GBM cell motility and monocyte adhesion are mediated by activation of the serine/threonine-specific protein kinase (AKT), focal adhesion kinase (FAK), and epidermal growth factor receptor (EGFR) signaling pathways. Moreover, hypoxia mediated the acetylated signal transducer and activator of transcription (STAT)3 expression and regulated the transcriptional activity of hypoxia inducible factor (HIF)-1α in GBM cell lines. In a GBM mouse model, MCT4 was significantly increased in the tumor necrotic tissues. These findings raise the possibility for the development of novel therapeutic strategies targeting MCT4.
Indexed as
Identifiers
What Socratic 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 Socratic graph.