Valeric acid from oral microbiome suppresses esophageal cancer growth by disrupting eEF1A1 -mediated translational output.

Yuanpeng He, Hao Peng, Lianglan Li, Siqi Sheng, Qi Wang, Weiqin Li, Fengqing Lin, Jun Yi

Abstract read

In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Yuanpeng He *Department of Cardiothoracic Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.

Hao Peng *Department of Cardiothoracic Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.

Lianglan Li *Department of Critical Care Medicine, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.

Siqi ShengDepartment of Medical Oncology, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.

Qi WangDepartment of Critical Care Medicine, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.

Weiqin LiDepartment of Critical Care Medicine, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China. liweiqindr@nju.edu.cn.

Fengqing LinDepartment of Critical Care Medicine, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China. 602022350068@smail.nju.edu.cn.ORCID http://orcid.org/0000-0003-2968-2802

Jun YiDepartment of Cardiothoracic Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China. dr.junyi@nju.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysbiosis of the oral microbiome has been associated with esophageal squamous cell carcinoma (ESCC), but how it impacts ESCC remains largely unknown. Surprisingly, we find that the oral microbiota derived from ESCC patients-not that from healthy controls-exhibits potent inhibitory and cytotoxic effects on ESCC cells. This anti-tumor effect is attributable to Veillonella, which is enriched in the ESCC-associated microbiota. Mechanistically, Veillonella produces valeric acid, which is transported into cells via MCT1 and inhibits the GTPase activity of eEF1A1, thereby suppressing protein translation. These findings identify valeric acid as a potential postbiotic for ESCC treatment and underscore the necessity of functional validation beyond observational and correlative studies.

Indexed as

Esophageal NeoplasmsMicrobiotaMouthPeptide Elongation Factor 1Protein BiosynthesisAnimalsCarcinoma, Squamous CellCell Line, TumorCell ProliferationEsophageal Squamous Cell CarcinomaHumansMiceMonocarboxylate Transport Protein 1EEF1A1 protein, humanMonocarboxylate Transport Protein 1Peptide Elongation Factor 1

Identifiers

PMID41896243

DOI10.1038/s41467-026-71209-1

PMCPMC13195117

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LicenceCC BY-NC-ND

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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.