Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMedOpen access

A Lamp2a-linked RNA secreted by ADSCs prevents ENO1-lactylation-glycolysis feedback and cell malignant behavior in triple-negative breast cancer.

Cheng S., Xia B., Li L., Zhao S., Zhang Q., Hui X.

Animal Study, published in Cell Death Dis (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Cell Death Dis (2026)
Country
England
Reported sample size
—
Source database
PubMed
PMID
41771848
PMCID
PMC13031273
DOI
10.1038/s41419-026-08517-3
Citations
1

Abstract (original English)

Triple-negative breast cancer (TNBC) is a subtype characterized by the absence of common BC receptors and is closely associated with a hypoxic tumor microenvironment. However, the mechanisms through which TNBCs adapt to hypoxia remain elusive. This study revealed elevated ENO1 levels in various BC datasets and revealed ENO1 protein lactylation in BC samples through 4D label-free lactylation quantitative proteomics analysis. The results indicated that lactylation increases ENO1 protein stability and enzyme activity, which promotes glycolysis. Notably, as lactate levels increased, a positive feedback loop was established, further promoting lactylation of ENO1. This positive feedback mechanism enables TNBC cells to adapt more efficiently to hypoxia and enhances their malignant behaviors. Lactylation prevented the lysosomal degradation of ENO1. In this study, the characteristics of ENO1, an RNA-binding protein, were assessed to determine how to interfere with its lactylation; specifically, an RNA ligand that can be specifically bound by ENO1 was identified. The RNA ligand was found to be linked to the Lamp2a protein in adipose stem cells (ADSCs) after stable transfection with Lamp2a-TAT and TRA-ligand plasmids. ADSCs seeded in a polyglycolic acid scaffold secreted exosomes containing the Lamp2a-linked ligand. This RNA ligand binds to ENO1 after it enters TNBC cells and further indu

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
HumansPhosphopyruvate HydrataseFemaleTriple Negative Breast NeoplasmsTumor Suppressor ProteinsDNA-Binding ProteinsGlycolysisCell Line, TumorLysosomal-Associated Membrane Protein 2Lactic Acid

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