Evidence map›Paper›PMID 41205595›Full record

ArticleCell reports. Medicine2025

Non-orthosteric inhibition of enolase 1 impedes growth of triple-negative breast cancer.

Dhanir Tailor, Fernando Jose Garcia-Marques, Abel Bermudez, Annah S Rolig, Benedikt Grau, Arpit Dheeraj, Dhanya K Nambiar, Wenqi Li, Kirsten Stefan, Shawn Campbell and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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.

Dhanir TailorDepartment of Cell, Developmental & Cancer Biology, Oregon Health & Science University, Portland, OR, USA; Center for Experimental Therapeutics, Oregon Health & Science University, Portland, OR, USA; Knight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.
Fernando Jose Garcia-MarquesDepartment of Radiology, Canary Center at Stanford for Cancer Early Detection, Stanford University School of Medicine, Palo Alto, CA 94304, USA.
Abel BermudezDepartment of Radiology, Canary Center at Stanford for Cancer Early Detection, Stanford University School of Medicine, Palo Alto, CA 94304, USA.
Annah S RoligDepartment of Cell, Developmental & Cancer Biology, Oregon Health & Science University, Portland, OR, USA; Center for Experimental Therapeutics, Oregon Health & Science University, Portland, OR, USA; Knight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.
Benedikt GrauDepartment of Cell, Developmental & Cancer Biology, Oregon Health & Science University, Portland, OR, USA; Center for Experimental Therapeutics, Oregon Health & Science University, Portland, OR, USA; Knight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.
Arpit DheerajDepartment of Cell, Developmental & Cancer Biology, Oregon Health & Science University, Portland, OR, USA; Center for Experimental Therapeutics, Oregon Health & Science University, Portland, OR, USA; Knight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.
Dhanya K NambiarDepartment of Radiation Oncology, Stanford University School of Medicine, Palo Alto, CA 94304, USA.
Wenqi LiDepartment of Cell, Developmental & Cancer Biology, Oregon Health & Science University, Portland, OR, USA; Center for Experimental Therapeutics, Oregon Health & Science University, Portland, OR, USA; Knight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.
Kirsten StefanDepartment of Cell, Developmental & Cancer Biology, Oregon Health & Science University, Portland, OR, USA; Center for Experimental Therapeutics, Oregon Health & Science University, Portland, OR, USA; Knight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.
Shawn CampbellDepartment of Cell, Developmental & Cancer Biology, Oregon Health & Science University, Portland, OR, USA; Center for Experimental Therapeutics, Oregon Health & Science University, Portland, OR, USA; Knight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.
Sharon J PitteriDepartment of Radiology, Canary Center at Stanford for Cancer Early Detection, Stanford University School of Medicine, Palo Alto, CA 94304, USA.
Sanjay V MalhotraDepartment of Cell, Developmental & Cancer Biology, Oregon Health & Science University, Portland, OR, USA; Center for Experimental Therapeutics, Oregon Health & Science University, Portland, OR, USA; Knight Cancer Institute, Oregon Health & Science University, Portland, OR, USA. Electronic address: malhotsa@ohsu.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells exploit and overexpress glycolytic enzymes such as enolase 1 (ENO1) to sustain the Warburg effect, a hallmark of cancer metabolism, which makes ENO1 a compelling therapeutic target. Here, we demonstrate that SU212, a small molecule inhibitor, binds ENO1 and induces its degradation, restricting its intracellular localization. Through these effects, SU212 reduces tumor cell glycolytic activity and glucose uptake and ultimately suppresses tumor growth and metastasis in syngeneic, genetic, and patient-derived xenograft models of triple-negative breast cancer. Further, in a diabetic mouse model, SU212 demonstrated robust anti-tumor efficacy while improving fatty liver conditions and lowering blood glucose. Other glycolytic enzyme inhibitors have been limited by toxicity; thorough pharmacokinetic and toxicity testing of SU212 revealed a favorable drug-like profile with minimal toxicity and no interference with key biological systems. These findings highlight SU212's dual-action potential to disrupt cancer metabolism and address metabolic disorders, offering a transformative approach to cancer therapy.

Indexed as

DNA-Binding ProteinsEnzyme InhibitorsPhosphopyruvate HydrataseTriple Negative Breast NeoplasmsTumor Suppressor ProteinsAnimalsBiomarkers, TumorCell Line, TumorCell ProliferationFemaleGlycolysisHumansMiceXenograft Model Antitumor AssaysBiomarkers, TumorDNA-Binding ProteinsENO1 protein, humanEnzyme InhibitorsPhosphopyruvate HydrataseTumor Suppressor ProteinsAza-podophyllotoxin derivativeENO1enolasenon-orthosteric inhibitiontriple-negative breast cancer

Identifiers

PMID41205595
PMCPMC12711674

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.