Evidence map›Paper›PMID 30545372›Full record

ArticleJournal of experimental & clinical cancer research : CR2018

The epigenetically downregulated factor CYGB suppresses breast cancer through inhibition of glucose metabolism.

Yixiao Feng, Mingjun Wu, Shuman Li, Xiaoqian He, Jun Tang, Weiyan Peng, Beilei Zeng, Chuxia Deng, Guosheng Ren, Tingxiu Xiang

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  8. Effects ofBreast cancer (Dove Medical Press) · 2025
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  16. Effect of differential hypoxia-related gene expression on glioblastoma.The Journal of international medical research · 2021
    Article
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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

10 authors at 4 institutions in 2 countries.

Yixiao FengChongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Mingjun WuInstitute of Life Science, Chongqing Medical University, Chongqing, China.
Shuman LiDepartment of Oncology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Xiaoqian HeChongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jun TangChongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Weiyan PengChongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Beilei ZengChongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Chuxia DengFaculty of Health Sciences, University of Macau, Macau SAR, China.
Guosheng RenChongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Tingxiu XiangChongqing Key Laboratory of Molecular Oncology and Epigenetics, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China. larissaxiang@163.com.
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CNDalian Medical University · CNUniversity of Macau · MO

Funding

NSFC #81372238NSFC #81572769
6 · The paper itself

Abstract

backgroundRecent studies suggested the globin family member cytoglobin (CYGB) as a potential tumor suppressor; however, the mechanism by which CYGB suppresses cancer is elusive. We investigated the role and mechanism of CYGB in suppressing breast cancer.

methodsCYGB expression was examined by reverse transcription PCR, quantitative reverse transcription PCR and open database analysis. Promoter methylation was examined by methylation-specific PCR. Metabolomics and proteomics were analyzed by gas chromatography-mass spectrometry and isobaric tags for relative and absolute quantitation, respectively. The effects and mechanisms of ectopic CYGB expression in breast cancer cells were assessed with molecular biological and cellular approaches in vitro and with a xenograft tumor model in nude mice.

resultsCYGB expression was downregulated in breast cancer tissues and cell lines, which was associated with promoter methylation. Ectopic CYGB expression suppressed proliferation, migration, invasion and induced apoptosis in breast cancer cell lines MCF7 (p53WT) and MB231 (p53mt) in vitro, and inhibited xenograft tumor growth in vivo. By proteomics and metabolomics analysis, glucose metabolism was found to be one of the main pathways suppressed by CYGB. The CYGB-expressing cells had lower ATP and compromised glycolysis. Additionally, CYGB suppressed key glucose metabolism factors including GLUT1 and HXK2 in p53-dependent and -independent manners. Restoration of GLUT1 or HXK2 expression attenuated CYGB-mediated proliferation suppression and apoptosis induction.

conclusionsCYGB is a potential tumor suppressor in breast cancer that is epigenetically suppressed. The results for the first time suggest that CYGB suppresses breast cancer through inhibiting glucose metabolism, which could be exploited for breast cancer prevention and therapy.

Indexed as

AnimalsApoptosisBreast NeoplasmsCell Cycle CheckpointsCell Line, TumorCell ProliferationCytoglobinDown-RegulationFemaleGlucoseHeterograftsHumansMCF-7 CellsMice, Inbred BALB CMice, NudeCYGB protein, humanCytoglobinGlucoseBreast cancerCYGBGLUT1GlycolysisHXK2Metabolismp53

Identifiers

PMID30545372
PMCPMC6293581
OpenAlexW2904177964

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.