Evidence map›Paper›PMID 30602670›Full record

ArticleCancers2018

Ovarian Cancer Relies on Glucose Transporter 1 to Fuel Glycolysis and Growth: Anti-Tumor Activity of BAY-876.

Yibao Ma, Wei Wang, Michael O Idowu, Unsong Oh, Xiang-Yang Wang, Sarah M Temkin, Xianjun Fang

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
4.1field-weighted citation impact, top 4% 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

92 citing papers in PubMed, 138 citations in OpenAlex.

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32 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

7 authors at 1 institution in 1 country.

Yibao MaDepartment of Biochemistry & Molecular Biology, Virginia Commonwealth University School of Medicine, 1101 East Marshall Street, Richmond, VA 23298, USA. yibao.ma@vcuhealth.org.
Wei WangDepartment of Biochemistry & Molecular Biology, Virginia Commonwealth University School of Medicine, 1101 East Marshall Street, Richmond, VA 23298, USA. wei.wang1@vcuhealth.org.
Michael O IdowuPathology, Virginia Commonwealth University School of Medicine, Richmond, VA 23298, USA. michael.idowu@vcuhealth.org.
Unsong OhNeurology, Virginia Commonwealth University School of Medicine, Richmond, VA 23298, USA. unsong.oh@vcuhealth.org.
Xiang-Yang WangHuman & Molecular Genetics, Virginia Commonwealth University School of Medicine, Richmond, VA 23298, USA. xiang-yang.wang@vcuhealth.org.
Sarah M TemkinGynecological Oncology, Virginia Commonwealth University School of Medicine, Richmond, VA 23298, USA. sarah.temkin@vcuhealth.org.
Xianjun FangDepartment of Biochemistry & Molecular Biology, Virginia Commonwealth University School of Medicine, 1101 East Marshall Street, Richmond, VA 23298, USA. xianjun.fang@vcuhealth.org.
Virginia Commonwealth University · US

Funding

Astar Biotechnology Research award N/ANational Institutes of Health P30 CA16059
6 · The paper itself

Abstract

The recent progresses in understanding of cancer glycolytic phenotype have offered new strategies to manage ovarian cancer and other malignancies. However, therapeutic targeting of glycolysis to treat cancer remains unsuccessful due to complex mechanisms of tumor glycolysis and the lack of selective, potent and safe glycolytic inhibitors. Recently, BAY-876 was identified as a new-generation inhibitor of glucose transporter 1 (GLUT1), a GLUT isoform commonly overexpressed but functionally poorly defined in ovarian cancer. Notably, BAY-876 has not been evaluated in any cell or preclinical animal models since its discovery. We herein took advantage of BAY-876 and molecular approaches to study GLUT1 regulation, targetability, and functional relevance to cancer glycolysis. The anti-tumor activity of BAY-876 was evaluated with ovarian cancer cell line- and patient-derived xenograft (PDX) models. Our results show that inhibition of GLUT1 is sufficient to block basal and stress-regulated glycolysis, and anchorage-dependent and independent growth of ovarian cancer cells. BAY-876 dramatically inhibits tumorigenicity of both cell line-derived xenografts and PDXs. These studies provide direct evidence that GLUT1 is causally linked to the glycolytic phenotype in ovarian cancer. BAY-876 is a potent blocker of GLUT1 activity, glycolytic metabolism and ovarian cancer growth, holding promise as a novel glycolysis-targeted anti-cancer agent.

Indexed as

BAY-876glucose transporter 1glycolysisovarian cancerpatient-derived xenograft

Identifiers

PMID30602670
PMCPMC6356953
OpenAlexW2907710771

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.