Evidence map›Paper›PMID 42196455›Full record

ReviewInternational journal of molecular sciences2026

ENO1 as a Central Regulator Linking Metabolic Reprogramming to Tumor Plasticity.

Tsung-Chieh Lin

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

1 author.

Tsung-Chieh LinGenomic Medicine Core Laboratory, Department of Medical Research and Development, Chang Gung Memorial Hospital, Linkou, Taoyuan City 333, Taiwan.ORCID 0000-0002-5985-3580

Funding

Chang Gung Memorial Hospital CMRPG3P0441
6 · The paper itself

Abstract

Alpha-enolase (ENO1) is a multifunctional protein best known for its canonical role in glycolysis, but growing evidence indicates that it also plays important roles in cancer development and progression. This review summarizes the current knowledge regarding the biological and clinical significance of ENO1 across multiple cancer types. We first outline the physiological characteristics of ENO1 and its distribution in normal tissues. Then, we discuss its aberrant expression patterns and genomic alterations in human cancers. We further examine the evidence linking ENO1 to major cancer-related processes, including proliferation, apoptosis resistance, cancer stemness, autophagy, metastasis, drug resistance, and angiogenesis. In addition, we review studies that evaluate the association between ENO1 expression and patient prognosis in pan-cancer datasets and individual malignancies. Collectively, the available literature indicates that ENO1 is closely associated with malignant progression through its involvement in metabolic reprogramming and broader tumor-promoting cellular functions. These findings suggest that ENO1 may serve as a context-dependent biomarker and a candidate therapeutic target in selected cancer settings; however, further mechanistic validation and clinically annotated studies are required before its translational value can be firmly established.

Indexed as

DNA-Binding ProteinsNeoplasmsPhosphopyruvate HydrataseTumor Suppressor ProteinsAnimalsBiomarkers, TumorGene Expression Regulation, NeoplasticHumansMetabolic ReprogrammingPrognosisBiomarkers, TumorDNA-Binding ProteinsENO1 protein, humanPhosphopyruvate HydrataseTumor Suppressor Proteinscancer metabolismdrug resistanceENO1metastasispan-cancer analysisprognostic biomarkertumor progression

Identifiers

PMID42196455
PMCPMC13208067

What OpenQuestion holds

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Registered trials

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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.