Evidence map›Paper›PMID 32641495›Full record

ReviewThe Journal of biological chemistry2020

Metabolite sensing and signaling in cancer.

Yi-Ping Wang, Jin-Tao Li, Jia Qu, Miao Yin, Qun-Ying Lei

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

Review in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.6field-weighted citation impact, top 5% 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

52 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Metabolite sensing receptors in macrophage reprogramming: from inflammation to resolution.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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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

5 authors at 1 institution in 1 country.

Yi-Ping WangFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Cancer Institutes, Key Laboratory of Breast Cancer in Shanghai, Shanghai Key Laboratory of Medical Epigenetics, and Shanghai Medical College, Fudan University, Shanghai, China yiping_wang@fudan.edu.cn qlei@fudan.edu.cn.
Jin-Tao LiFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Cancer Institutes, Key Laboratory of Breast Cancer in Shanghai, Shanghai Key Laboratory of Medical Epigenetics, and Shanghai Medical College, Fudan University, Shanghai, China.
Jia QuFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Cancer Institutes, Key Laboratory of Breast Cancer in Shanghai, Shanghai Key Laboratory of Medical Epigenetics, and Shanghai Medical College, Fudan University, Shanghai, China.
Miao YinFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Cancer Institutes, Key Laboratory of Breast Cancer in Shanghai, Shanghai Key Laboratory of Medical Epigenetics, and Shanghai Medical College, Fudan University, Shanghai, China.
Qun-Ying LeiFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Cancer Institutes, Key Laboratory of Breast Cancer in Shanghai, Shanghai Key Laboratory of Medical Epigenetics, and Shanghai Medical College, Fudan University, Shanghai, China yiping_wang@fudan.edu.cn qlei@fudan.edu.cn.ORCID 0000-0002-8547-8518
Shanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolites are not only substrates in metabolic reactions, but also signaling molecules controlling a wide range of cellular processes. Discovery of the oncometabolite 2-hydroxyglutarate provides an important link between metabolic dysfunction and cancer, unveiling the signaling function of metabolites in regulating epigenetic and epitranscriptomic modifications, genome integrity, and signal transduction. It is now known that cancer cells remodel their metabolic network to support biogenesis, caused by or resulting in the dysregulation of various metabolites. Cancer cells can sense alterations in metabolic intermediates to better coordinate multiple biological processes and enhance cell metabolism. Recent studies have demonstrated that metabolite signaling is involved in the regulation of malignant transformation, cell proliferation, epithelial-to-mesenchymal transition, differentiation blockade, and cancer stemness. Additionally, intercellular metabolite signaling modulates inflammatory response and immunosurveillance in the tumor microenvironment. Here, we review recent advances in cancer-associated metabolite signaling. An in depth understanding of metabolite signaling will provide new opportunities for the development of therapeutic interventions that target cancer.

Indexed as

Metabolic Networks and PathwaysMetabolomeAnimalsEpigenesis, GeneticGlutaratesHumansMetabolomicsNeoplasmsSignal TransductionTumor Microenvironmentalpha-hydroxyglutarateGlutarates2HGcancercancer biologycancer stem cellsimmunosurveillancemetabolic diseasemetabolic intermediatemetabolic regulationmetabolitemetabolite sensingmetabolomicsoncogenic signalingoncometabolitesensingsignalingsignal transductiontumor metabolismtumor microenvironment

Identifiers

PMID32641495
PMCPMC7450124
OpenAlexW3041991893

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.