Evidence map›Paper›PMID 35544303›Full record

ArticleMolecular biology of the cell2022

The short-chain fatty acid acetate modulates epithelial-to-mesenchymal transition.

Junfang Lyu, Mehdi Pirooznia, Yuesheng Li, Jianhua Xiong

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed.

  1. Reversible alterations of brain acetate metabolism associated with alcohol consumption.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Acetate Metabolism in Urological Health and Disease.Serican journal of medicine · 2024
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Junfang LyuDepartment of Medicine, Division of Endocrinology, Diabetes and Metabolism, Johns Hopkins University School of Medicine, St. Petersburg, FL 33701.
Mehdi PiroozniaNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Yuesheng LiNational Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Jianhua XiongDepartment of Medicine, Division of Endocrinology, Diabetes and Metabolism, Johns Hopkins University School of Medicine, St. Petersburg, FL 33701.

Funding

Mechanisms and functions of fatty acid oxidation in T cell differentiationK22HL146793 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI XIONG, JIANHUA · 2022 to 2024
$747k
NHLBI NIH HHS K22 HL146793
6 · The paper itself

Abstract

Normal tissue and organ morphogenesis requires epithelial cell plasticity and conversion to a mesenchymal phenotype through a tightly regulated process-epithelial-to-mesenchymal transition (EMT). Alterations of EMT go far beyond cell-lineage segregation and contribute to pathologic conditions such as cancer. EMT is subject to intersecting control pathways; however, EMT's metabolic mechanism remains poorly understood. Here, we demonstrate that transforming growth factor β (TGF-β)-induced EMT is accompanied by decreased fatty acid oxidation (FAO) and reduced acetyl-coenzyme A (acetyl-CoA) levels. Acetyl-CoA is a central metabolite and the sole donor of acetyl groups to acetylate key proteins. Further, the short-chain fatty acid acetate increases acetyl-CoA levels--robustly inhibiting EMT and cancer cell migration. Acetate can restore EMT-associated α-tubulin acetylation levels, increasing microtubule stability. Transcriptome profiling and flow cytometric analysis show that acetate inhibits the global gene expression program associated with EMT and the EMT-associated G1 cell cycle arrest. Taken together, these results demonstrate that acetate is a potent metabolic regulator of EMT and that therapeutic manipulation of acetate metabolism could provide the basis for treating a wide range of EMT-linked pathological conditions, including cancer.

Indexed as

Epithelial-Mesenchymal TransitionTransforming Growth Factor betaAcetatesAcetyl Coenzyme AFatty Acids, VolatileAcetatesAcetyl Coenzyme AFatty Acids, VolatileTransforming Growth Factor beta

Identifiers

PMID35544303
PMCPMC9635288

What Socratic holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.