Evidence map›Paper›PMID 25603933›Full record

ArticleThe EMBO journal2015

miR-290/371-Mbd2-Myc circuit regulates glycolytic metabolism to promote pluripotency.

Yang Cao, Wen-Ting Guo, Shengya Tian, Xiaoping He, Xi-Wen Wang, Xiaomeng Liu, Kai-Li Gu, Xiaoyu Ma, De Huang, Lan Hu and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
4.6field-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

59 citing papers in PubMed, 91 citations in OpenAlex.

  1. Genes, fuel, and fate in lung cancer.Biochemical Society transactions · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Myc beyond Cancer: Regulation of Mammalian Tissue Regeneration.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023
    Review
  11. Article
  12. Review
  13. Metabolic control of induced pluripotency.Frontiers in cell and developmental biology · 2023
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Role of metabolic reprogramming in drug resistance to epidermal growth factor tyrosine kinase inhibitors in non-small cell lung cancer.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021
    Article
  20. Article
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

14 authors at 4 institutions in 1 country.

Yang CaoThe CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Biology, School of Life Sciences, University of Science and Technology of China, Hefei, China.
Wen-Ting GuoBeijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Peking University, Beijing, China.
Shengya TianThe CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Biology, School of Life Sciences, University of Science and Technology of China, Hefei, China.
Xiaoping HeThe CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Biology, School of Life Sciences, University of Science and Technology of China, Hefei, China.
Xi-Wen WangBeijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Peking University, Beijing, China.
Xiaomeng LiuBiodynamic Optical Imaging Center, College of Life Sciences, Peking University, Beijing, China.
Kai-Li GuBeijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Peking University, Beijing, China.
Xiaoyu MaThe CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Biology, School of Life Sciences, University of Science and Technology of China, Hefei, China.
De HuangThe CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Biology, School of Life Sciences, University of Science and Technology of China, Hefei, China.
Lan HuThe CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Biology, School of Life Sciences, University of Science and Technology of China, Hefei, China.
Yongping CaiDepartment of Pathology, School of Medicine, Anhui Medical University, Hefei, China.
Huafeng ZhangThe CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Biology, School of Life Sciences, University of Science and Technology of China, Hefei, China.
Yangming WangBeijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Peking University, Beijing, China yangming.wang@pku.edu.cn pgao2@ustc.edu.cn.
Ping GaoThe CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Biology, School of Life Sciences, University of Science and Technology of China, Hefei, China yangming.wang@pku.edu.cn pgao2@ustc.edu.cn.
University of Science and Technology of China · CNCenter for Life Sciences · CNPeking University · CNAnhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enhanced glycolysis is a main feature of pluripotent stem cells (PSCs) and is proposed to be important for the maintenance and induction of pluripotency. The molecular mechanism underlying enhanced glycolysis in PSCs is not clear. Using Dgcr8-/- mouse embryonic stem cells (ESCs) that lack mature miRNAs, we found that miR-290 cluster of miRNAs stimulates glycolysis by upregulating glycolytic enzymes Pkm2 and Ldha, which are also essential for the induction of pluripotency during reprogramming. Mechanistically, we identified Mbd2, a reader for methylated CpGs, as the target of miR-290 cluster that represses glycolysis and reprogramming. Furthermore, we discovered Myc as a key target of Mbd2 that controls metabolic switch in ESCs. Importantly, we demonstrated that miR-371 cluster, a human homolog of miR-290 cluster, stimulates glycolysis to promote the reprogramming of human fibroblasts. Hence, we identified a previously unappreciated mechanism by which miR-290/371 miRNAs orchestrate epigenetic, transcriptional and metabolic networks to promote pluripotency in PSCs and during reprogramming.

Indexed as

AnimalsChromatin ImmunoprecipitationDNA-Binding ProteinsDNA PrimersGene Knockout TechniquesGlycolysisMetabolic Networks and PathwaysMiceMice, KnockoutMicroRNAsPluripotent Stem CellsProto-Oncogene Proteins c-mycReverse Transcriptase Polymerase Chain ReactionRNA-Binding ProteinsRNA, Small InterferingDgcr8 protein, mouseDNA-Binding ProteinsDNA PrimersMbd2 protein, mouseMicroRNAsMIRN290 microRNA, mouseMyc protein, mouseProto-Oncogene Proteins c-mycRNA-Binding ProteinsRNA, Small InterferingglycolysisMbd2metabolismmicroRNApluripotency

Identifiers

PMID25603933
PMCPMC4365031
OpenAlexW2158325162

What OpenQuestion holds

Textmetadata
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.