Evidence map›Paper›PMID 25609694›Full record

ArticleNucleic acids research2015

ZBTB2 increases PDK4 expression by transcriptional repression of RelA/p65.

Min-Young Kim, Dong-In Koh, Won-Il Choi, Bu-Nam Jeon, Deok-yoon Jeong, Kyung-Sup Kim, Kunhong Kim, Se-Hoon Kim, Man-Wook Hur

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

23 citing papers in PubMed, 47 citations in OpenAlex.

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  7. Pathogens (Basel, Switzerland) · 2023
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  9. SP and KLF Transcription Factors in Cancer Metabolism.International journal of molecular sciences · 2022
    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

9 authors at 1 institution in 1 country.

Min-Young KimDepartment of Biochemistry and Molecular Biology, Brain Korea 21 Plus Project for Medical Science, Severance Biomedical Research Institute, Yonsei University School of Medicine, 50-1 Yonsei-Ro, SeoDaeMun-Gu, Seoul 120-752, Korea.
Dong-In KohDepartment of Biochemistry and Molecular Biology, Brain Korea 21 Plus Project for Medical Science, Severance Biomedical Research Institute, Yonsei University School of Medicine, 50-1 Yonsei-Ro, SeoDaeMun-Gu, Seoul 120-752, Korea.
Won-Il ChoiDepartment of Biochemistry and Molecular Biology, Brain Korea 21 Plus Project for Medical Science, Severance Biomedical Research Institute, Yonsei University School of Medicine, 50-1 Yonsei-Ro, SeoDaeMun-Gu, Seoul 120-752, Korea.
Bu-Nam JeonDepartment of Biochemistry and Molecular Biology, Brain Korea 21 Plus Project for Medical Science, Severance Biomedical Research Institute, Yonsei University School of Medicine, 50-1 Yonsei-Ro, SeoDaeMun-Gu, Seoul 120-752, Korea.
Deok-yoon JeongDepartment of Biochemistry and Molecular Biology, Brain Korea 21 Plus Project for Medical Science, Severance Biomedical Research Institute, Yonsei University School of Medicine, 50-1 Yonsei-Ro, SeoDaeMun-Gu, Seoul 120-752, Korea.
Kyung-Sup KimDepartment of Biochemistry and Molecular Biology, Brain Korea 21 Plus Project for Medical Science, Severance Biomedical Research Institute, Yonsei University School of Medicine, 50-1 Yonsei-Ro, SeoDaeMun-Gu, Seoul 120-752, Korea.
Kunhong KimDepartment of Biochemistry and Molecular Biology, Brain Korea 21 Plus Project for Medical Science, Severance Biomedical Research Institute, Yonsei University School of Medicine, 50-1 Yonsei-Ro, SeoDaeMun-Gu, Seoul 120-752, Korea.
Se-Hoon KimDepartment of Pathology, Yonsei University School of Medicine, 50-1 Yonsei-Ro, SeoDaeMun-Gu, Seoul 120-752, Korea.
Man-Wook HurDepartment of Biochemistry and Molecular Biology, Brain Korea 21 Plus Project for Medical Science, Severance Biomedical Research Institute, Yonsei University School of Medicine, 50-1 Yonsei-Ro, SeoDaeMun-Gu, Seoul 120-752, Korea mwhur2@yuhs.ac.
Yonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The NF-κB is found in almost all animal cell types and is involved in a myriad of cellular responses. Aberrant expression of NF-κB has been linked to cancer, inflammatory diseases and improper development. Little is known about transcriptional regulation of the NF-κB family member gene RelA/p65. Sp1 plays a key role in the expression of the RelA/p65 gene. ZBTB2 represses transcription of the gene by inhibiting Sp1 binding to a Sp1-binding GC-box in the RelA/p65 proximal promoter (bp, -31 to -21). Moreover, recent studies revealed that RelA/p65 directly binds to the peroxisome proliferator-activated receptor-γ coactivator1α (PGC1α) to decrease transcriptional activation of the PGC1α target gene PDK4, whose gene product inhibits pyruvate dehydrogenase (PDH), a key regulator of TCA cycle flux. Accordingly, we observed that RelA/p65 repression by ZBTB2 indirectly results in increased PDK4 expression, which inhibits PDH. Consequently, in cells with ectopic ZBTB2, the concentrations of pyruvate and lactate were higher than those in normal cells, indicating changes in glucose metabolism flux favoring glycolysis over the TCA cycle. Knockdown of ZBTB2 in mouse xenografts decreased tumor growth. ZBTB2 may increase cell proliferation by reprogramming glucose metabolic pathways to favor glycolysis by upregulating PDK4 expression via repression of RelA/p65 expression.

Indexed as

Transcription, GeneticBase SequenceCell LineDNA PrimersHumansPromoter Regions, GeneticProtein Serine-Threonine KinasesPyruvate Dehydrogenase Acetyl-Transferring KinaseReal-Time Polymerase Chain ReactionRepressor ProteinsSp1 Transcription FactorTranscription Factor RelADNA PrimersPDK4 protein, humanPdk4 protein, mouseProtein Serine-Threonine KinasesPyruvate Dehydrogenase Acetyl-Transferring KinaseRepressor ProteinsSp1 Transcription FactorTranscription Factor RelAZBTB2 protein, human

Identifiers

PMID25609694
PMCPMC4330387
OpenAlexW2139351795

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

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.