Evidence map›Paper›PMID 29677490›Full record

ArticleMolecular cell2018

EGFR-Phosphorylated Platelet Isoform of Phosphofructokinase 1 Promotes PI3K Activation.

Jong-Ho Lee, Rui Liu, Jing Li, Yugang Wang, Lin Tan, Xin-Jian Li, Xu Qian, Chuanbao Zhang, Yan Xia, Daqian Xu and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed, 2 pooled it
4.9field-weighted citation impact, top 3% 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

130 citing papers in PubMed, 2 syntheses or guidelines pooled it, 214 citations in OpenAlex.

  1. Pooled it
  2. Interplay Between Glucose Metabolism and Chromatin Modifications in Cancer.Frontiers in cell and developmental biology · 2021
    Pooled it
  3. Article
  4. Metabolic-epigenetic reprogrammingActa pharmaceutica Sinica. B · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Unraveling the role of specificity protein 1 in gliomas: pathophysiology and clinical implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  9. Review
  10. Article
  11. The moonlighting functions of glycolytic enzymes in tumorigenesis.Cellular oncology (Dordrecht, Netherlands) · 2026
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. A Covalent PFKL Activator Suppresses Tumor Growth.bioRxiv : the preprint server for biology · 2025
    Article

70 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

19 authors at 4 institutions in 2 countries.

Jong-Ho LeeBrain Tumor Center and Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Rui LiuBrain Tumor Center and Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA; State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, China.
Jing LiBrain Tumor Center and Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA; State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, China.
Yugang WangBrain Tumor Center and Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Lin TanDepartment of Bioinformatics and Computational Biology and The Proteomics and Metabolomics Core Facility, The University of Texas MD Anderson Cancer Center, Houston, Texas 77054, USA.
Xin-Jian LiBrain Tumor Center and Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Xu QianBrain Tumor Center and Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Chuanbao ZhangBeijing Neurosurgical Institute, Capital Medical University, Beijing 100050, China.
Yan XiaBrain Tumor Center and Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Daqian XuBrain Tumor Center and Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Wei GuoDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Zhiyong DingDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Linyong DuBrain Tumor Center and Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Yanhua ZhengBrain Tumor Center and Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Qianming ChenState Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, China.
Philip L LorenziDepartment of Bioinformatics and Computational Biology and The Proteomics and Metabolomics Core Facility, The University of Texas MD Anderson Cancer Center, Houston, Texas 77054, USA.
Gordon B MillsDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Tao JiangBeijing Neurosurgical Institute, Capital Medical University, Beijing 100050, China.
Zhimin LuBrain Tumor Center and Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA; Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA; Cancer Biology Program, MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences, The University of Texas, Houston, Texas 77030, USA. Electronic address: zhiminlu@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USBeijing Institute of Neurosurgery · CNSichuan University · CNThe University of Texas Health Science Center at Houston · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Tropism Enhanced Oncolytic Adenovirus for the Treatment of Brain TumorsP50CA127001 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Juan Fueyo · 2008 to 2026
$41.2M
The Role of b-catenin in EGFR-Related Tumor DevelopmentR01CA109035 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LU, ZHIMIN · 2005 to 2016
$2.7M
The Mechanisms of PKM2-Regulated Gene Expression in Tumor Development.R01CA169603 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LU, ZHIMIN · 2013 to 2017
$1.7M
Deciphering the role of Cdc25A in cancer metabolism.R01NS089754 · NINDS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LU, ZHIMIN · 2015 to 2017
$1.1M
Orbitrap Elite High-Resolution Mass Spectrometer for Proteomics and MetabolomicsS10OD012304 · OD · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HAWKE, DAVID H · 2013 to 2013
$877k
NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA127001NCI NIH HHS R01 CA109035NCI NIH HHS R01 CA169603NIH HHS S10 OD012304NINDS NIH HHS R01 NS089754
6 · The paper itself

Abstract

EGFR activates phosphatidylinositide 3-kinase (PI3K), but the mechanism underlying this activation is not completely understood. We demonstrated here that EGFR activation resulted in lysine acetyltransferase 5 (KAT5)-mediated K395 acetylation of the platelet isoform of phosphofructokinase 1 (PFKP) and subsequent translocation of PFKP to the plasma membrane, where the PFKP was phosphorylated at Y64 by EGFR. Phosphorylated PFKP binds to the N-terminal SH2 domain of p85α, which is distinct from binding of Gab1 to the C-terminal SH2 domain of p85α, and recruited p85α to the plasma membrane resulting in PI3K activation. PI3K-dependent AKT activation results in enhanced phosphofructokinase 2 (PFK2) phosphorylation and production of fructose-2,6-bisphosphate, which in turn promotes PFK1 activation. PFKP Y64 phosphorylation-enhanced PI3K/AKT-dependent PFK1 activation and GLUT1 expression promoted the Warburg effect, tumor cell proliferation, and brain tumorigenesis. These findings underscore the instrumental role of PFKP in PI3K activation and enhanced glycolysis through PI3K/AKT-dependent positive-feedback regulation.

Indexed as

GlycolysisAcetylationAdaptor Proteins, Signal TransducingAnimalsBrain NeoplasmsCell Line, TumorClass Ia Phosphatidylinositol 3-KinaseEnzyme ActivationErbB ReceptorsFeedback, PhysiologicalFructosediphosphatesGlioblastomaGlucose Transporter Type 1HumansLysine Acetyltransferase 5MaleAdaptor Proteins, Signal TransducingClass Ia Phosphatidylinositol 3-KinaseEGFR protein, humanErbB Receptorsfructose 2,6-diphosphateFructosediphosphatesGAB1 protein, humanGlucose Transporter Type 1KAT5 protein, humanLysine Acetyltransferase 5PFKP protein, humanPhosphatidylinositol 3-KinasesPhosphofructokinase-1, Type CPhosphofructokinase-2PIK3R1 protein, humanProto-Oncogene Proteins c-aktSLC2A1 protein, humanEGFRPFKPphosphorylationPI3Kthe Warburg effect

Identifiers

PMID29677490
PMCPMC6114939
OpenAlexW2801789151

What OpenQuestion holds

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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.