Evidence map›Paper›PMID 31627130›Full record

ArticleiScience2019

Phosphofructokinases Axis Controls Glucose-Dependent mTORC1 Activation Driven by E2F1.

Eugènia Almacellas, Joffrey Pelletier, Anna Manzano, Antonio Gentilella, Santiago Ambrosio, Caroline Mauvezin, Albert Tauler

Open access · goldAbstract read
In one paragraph

Article in iScience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. METTL1-mediated mOncogene · 2026
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  11. Lysosomal glucose sensing and glycophagy in metabolism.Trends in endocrinology and metabolism: TEM · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. PFKP: More than phosphofructokinase.Advances in cancer research · 2023
    Review
  17. Article
  18. Circular RNA circ-FoxO3 attenuates blood-brain barrier damage by inducing autophagy during ischemia/reperfusion.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  19. Lysosomes at the Crossroads of Cell Metabolism, Cell Cycle, and Stemness.International journal of molecular sciences · 2022
    Review
  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

7 authors at 2 institutions in 1 country.

Eugènia AlmacellasDepartment of Biochemistry and Physiology, School of Pharmacy, University of Barcelona, Barcelona, Catalonia 08028, Spain; Laboratory of Cancer Metabolism, Molecular Mechanisms and Experimental Therapy in Oncology Program (Oncobell), Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), Hospitalet del Llobregat, Barcelona, Catalonia 08908, Spain.
Joffrey PelletierLaboratory of Cancer Metabolism, Molecular Mechanisms and Experimental Therapy in Oncology Program (Oncobell), Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), Hospitalet del Llobregat, Barcelona, Catalonia 08908, Spain.
Anna ManzanoBiochemistry Unit, Physiological Sciences Department, Faculty of Medicine and Health Science, University of Barcelona (IDIBELL), Hospitalet del Llobregat, Barcelona, Catalonia 08907, Spain.
Antonio GentilellaDepartment of Biochemistry and Physiology, School of Pharmacy, University of Barcelona, Barcelona, Catalonia 08028, Spain; Laboratory of Cancer Metabolism, Molecular Mechanisms and Experimental Therapy in Oncology Program (Oncobell), Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), Hospitalet del Llobregat, Barcelona, Catalonia 08908, Spain.
Santiago AmbrosioBiochemistry Unit, Physiological Sciences Department, Faculty of Medicine and Health Science, University of Barcelona (IDIBELL), Hospitalet del Llobregat, Barcelona, Catalonia 08907, Spain.
Caroline MauvezinLaboratory of Cancer Metabolism, Molecular Mechanisms and Experimental Therapy in Oncology Program (Oncobell), Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), Hospitalet del Llobregat, Barcelona, Catalonia 08908, Spain. Electronic address: cmauvezin@idibell.cat.
Albert TaulerDepartment of Biochemistry and Physiology, School of Pharmacy, University of Barcelona, Barcelona, Catalonia 08028, Spain; Laboratory of Cancer Metabolism, Molecular Mechanisms and Experimental Therapy in Oncology Program (Oncobell), Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), Hospitalet del Llobregat, Barcelona, Catalonia 08908, Spain. Electronic address: tauler@ub.edu.
Institut d'Investigació Biomédica de Bellvitge · ESUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells rely on mTORC1 activity to coordinate mitogenic signaling with nutrients availability for growth. Based on the metabolic function of E2F1, we hypothesize that glucose catabolism driven by E2F1 could participate on mTORC1 activation. Here, we demonstrate that glucose potentiates E2F1-induced mTORC1 activation by promoting mTORC1 translocation to lysosomes, a process that occurs independently of AMPK activation. We showed that E2F1 regulates glucose metabolism by increasing aerobic glycolysis and identified the PFKFB3 regulatory enzyme as an E2F1-regulated gene important for mTORC1 activation. Furthermore, PFKFB3 and PFK1 were found associated to lysosomes and we demonstrated that modulation of PFKFB3 activity, either by substrate accessibility or expression, regulates the translocation of mTORC1 to lysosomes by direct interaction with Rag B and subsequent mTORC1 activity. Our results support a model whereby a glycolytic metabolon containing phosphofructokinases transiently interacts with the lysosome acting as a sensor platform for glucose catabolism toward mTORC1 activity.

Indexed as

Cell BiologyMolecular Genetics

Identifiers

PMID31627130
PMCPMC6818336
OpenAlexW2945494553

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.