Evidence map›Paper›PMID 29739823›Full record

ArticleMolecular & cellular proteomics : MCP2018

Butyrate Suppresses the Proliferation of Colorectal Cancer Cells via Targeting Pyruvate Kinase M2 and Metabolic Reprogramming.

Qingran Li, Lijuan Cao, Yang Tian, Pei Zhang, Chujie Ding, Wenjie Lu, Chenxi Jia, Chang Shao, Wenyue Liu, Dong Wang and 2 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 2 pooled it
2.7field-weighted citation impact, top 9% of its field
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

84 citing papers in PubMed, 2 syntheses or guidelines pooled it, 139 citations in OpenAlex.

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  7. iScience · 2026
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  10. Preventive Effect of Butyrate in Colon Cancer Cell Metabolism.International journal of molecular sciences · 2026
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24 more citing papers are in PubMed but not listed here.

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

12 authors at 2 institutions in 1 country.

Qingran LiFrom the ‡Key Laboratory of Drug Metabolism and Pharmacokinetics, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Lijuan CaoFrom the ‡Key Laboratory of Drug Metabolism and Pharmacokinetics, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Yang TianFrom the ‡Key Laboratory of Drug Metabolism and Pharmacokinetics, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Pei Zhang§National Center for Protein Sciences-Beijing, State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing 102206, China.
Chujie DingFrom the ‡Key Laboratory of Drug Metabolism and Pharmacokinetics, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Wenjie LuFrom the ‡Key Laboratory of Drug Metabolism and Pharmacokinetics, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.ORCID 0000-0002-9732-5623
Chenxi Jia§National Center for Protein Sciences-Beijing, State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing 102206, China.
Chang ShaoFrom the ‡Key Laboratory of Drug Metabolism and Pharmacokinetics, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Wenyue LiuFrom the ‡Key Laboratory of Drug Metabolism and Pharmacokinetics, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Dong WangFrom the ‡Key Laboratory of Drug Metabolism and Pharmacokinetics, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Hui YeFrom the ‡Key Laboratory of Drug Metabolism and Pharmacokinetics, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China; haipinghao@cpu.edu.cn cpuyehui@cpu.edu.cn.ORCID 0000-0002-7416-1558
Haiping HaoFrom the ‡Key Laboratory of Drug Metabolism and Pharmacokinetics, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China; haipinghao@cpu.edu.cn cpuyehui@cpu.edu.cn.
China Pharmaceutical University · CNBeijing Proteome Research Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Butyrate is a short chain fatty acid present in a high concentration in the gut lumen. It has been well documented that butyrate, by serving as an energetic metabolite, promotes the proliferation of normal colonocytes while, by serving as a histone deacetylase inhibitor, epigenetically suppressing the proliferation of cancerous counterparts undergoing the Warburg effect. However, how butyrate interrupts the metabolism of colorectal cancer cells and ultimately leads to the suppression of cell proliferation remains unclear. Here, we employed a metabolomics-proteomics combined approach to explore the link between butyrate-mediated proliferation arrest and cell metabolism. A metabolomics study revealed a remodeled metabolic profile with pronounced accumulation of pyruvate, decreased glycolytic intermediates upstream of pyruvate and reduced levels of nucleotides in butyrate-treated HCT-116 cells. Supplementation of key metabolite intermediates directly affected cancer-cell metabolism and modulated the suppressive effect of butyrate in HCT-116 cells. By a Drug Affinity Responsive Target Stability (DARTS)-based quantitative proteomics approach, we revealed the M2 isoform of a pyruvate kinase, PKM2, as a direct binding target of butyrate. Butyrate activates PKM2 via promoting its dephosphorylation and tetramerization and thereby reprograms the metabolism of colorectal cancer cells, inhibiting the Warburg effect while favoring energetic metabolism. Our study thus provides a mechanistic link between PKM2-induced metabolic remodeling and the antitumorigenic function of butyrate and demonstrates a widely applicable approach to uncovering unknown protein targets for small molecules with biological functions.

Indexed as

ButyratesCell Line, TumorCell ProliferationColorectal NeoplasmsEnzyme ActivationGlycolysisHumansModels, BiologicalPhosphorylationProtein MultimerizationProteomicsPyruvate KinaseButyratesPyruvate KinaseButyrateColorectal cancerDrug Affinity Responsive Target Stability (DARTS)Drug targetsMass SpectrometryMetabolic reprogrammingMetabolomicsProliferationPyruvate kinase M2Quantitative proteomicsTarget identification

Identifiers

PMID29739823
PMCPMC6072541
OpenAlexW2799897236

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.