ArticleDiscover oncology2025
LAMB1 downregulation suppresses glioma progression by inhibiting aerobic glycolysis through regulation of the NF-κB/HK2 axis.
Article in Discover oncology, 2025. 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 3 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
3 citing papers in PubMed.
- Identification and Integration of LRG1-Induced Differentially Expressed Gene (DEG) Hub Profiles in Breast Cancer Cells.International journal of molecular sciences · 2026Article
- Extracellular Vesicle-Mediated Regulation of H3C14 Contributes to Gemcitabine Resistance in Bladder Cancer.Journal of extracellular vesicles · 2025Article
- Correction: LAMB1 downregulation suppresses glioma progression by inhibiting aerobic glycolysis through regulation of the NF-κB/HK2 axis.Discover oncology · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors.
Funding
Abstract
backgroundLaminin subunit beta 1 (LAMB1) has regulatory functions on the proliferation, attachment, and migration of tumor cells, with increased levels linked to different cancers.
objectiveThis study aims at investigating the effects and mechanisms of LAMB1 in glioma. METHODS AND MATERIAL: Glioma cell models with LAMB1 overexpression or downregulation were constructed. Cell viability, proliferation, and invasion were evaluated. Glucose uptake and lactate production were examined, and Seahorse was used to assess the extracellular acidification rate (ECAR). The EC50 of temozolomide (TMZ) in glioma cells was tested. Western blotting was conducted to monitor the expression of HK1, HK2, PDHA, and PKM. Bioinformatic analysis was employed to investigate the downstream mechanism of LAMB1. In addition, a subcutaneous tumor model was constructed to determine the influence of LAMB1 on GBM cell growth in vivo.
resultsLAMB1 overexpression enhanced cell viability, proliferation, and invasion and promoted glioma cell growth. LAMB1 upregulation enhanced cellular glycolysis and repressed the sensitivity of cells to TMZ. LAMB1 activated the NF-κB pathway. Downregulation of LAMB1 or mitigating of the NF-κB pathway by Bay 11-7082 inhibited glioma cell proliferation, growth, and glycolysis and enhanced TMZ sensitivity.
conclusionsLAMB1 downregulation exerted antitumor effects on glioma cells by regulating the NF-κB/HK2 axis.
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Registered trials
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