Evidence map›Paper›PMID 25770584›Full record

ArticleThe EMBO journal2015

Che-1-induced inhibition of mTOR pathway enables stress-induced autophagy.

Agata Desantis, Tiziana Bruno, Valeria Catena, Francesca De Nicola, Frauke Goeman, Simona Iezzi, Cristina Sorino, Maurilio Ponzoni, Gianluca Bossi, Vincenzo Federico and 14 more

Open access · greenAbstract 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 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
6.5field-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

40 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Autophagy-related mechanisms for treatment of multiple myeloma.Cancer drug resistance (Alhambra, Calif.) · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. CK2-mediated phosphorylation of Che-1/AATF is required for its pro-proliferative activity.Journal of experimental & clinical cancer research : CR · 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

24 authors at 7 institutions in 3 countries.

Agata DesantisEpigenetics Laboratory, Molecular Medicine Area Regina Elena National Cancer Institute, Rome, Italy.
Tiziana BrunoEpigenetics Laboratory, Molecular Medicine Area Regina Elena National Cancer Institute, Rome, Italy.
Valeria CatenaEpigenetics Laboratory, Molecular Medicine Area Regina Elena National Cancer Institute, Rome, Italy Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy.
Francesca De NicolaEpigenetics Laboratory, Molecular Medicine Area Regina Elena National Cancer Institute, Rome, Italy.
Frauke GoemanTranslational Oncogenomic Laboratory, Molecular Medicine Area Regina Elena National Cancer Institute, Rome, Italy.
Simona IezziEpigenetics Laboratory, Molecular Medicine Area Regina Elena National Cancer Institute, Rome, Italy.
Cristina SorinoEpigenetics Laboratory, Molecular Medicine Area Regina Elena National Cancer Institute, Rome, Italy.
Maurilio PonzoniPathology and Myeloma Units, Molecular Oncology Division, San Raffaele Scientific Institute, Milan, Italy.
Gianluca BossiMolecular Oncogenesis Laboratory, Regina Elena National Cancer Institute, Rome, Italy.
Vincenzo FedericoDivision of Hematology, Department of Cellular Biotechnologies and Hematology, "Sapienza" University, Rome, Italy.
Francesca La RosaEpigenetics Laboratory, Molecular Medicine Area Regina Elena National Cancer Institute, Rome, Italy.
Maria Rosaria RicciardiDivision of Hematology, Department of Cellular Biotechnologies and Hematology, "Sapienza" University, Rome, Italy.
Elena LesmaLaboratory of Pharmacology, Department of Health Sciences, University of Milan, Milan, Italy.
Paolo D'Onorio De MeoHPC CINECA, Rome, Italy.
Tiziana CastrignanòHPC CINECA, Rome, Italy.
Maria Teresa PetrucciDivision of Hematology, Department of Cellular Biotechnologies and Hematology, "Sapienza" University, Rome, Italy.
Francesco PisaniHematology Laboratory, Regina Elena National Cancer Institute, Rome, Italy.
Marta ChesiComprehensive Cancer Center, Mayo Clinic Arizona, Scottsdale, AZ, USA.
P Leif BergsagelComprehensive Cancer Center, Mayo Clinic Arizona, Scottsdale, AZ, USA.
Aristide FloridiEpigenetics Laboratory, Molecular Medicine Area Regina Elena National Cancer Institute, Rome, Italy.
Giovanni TononFunctional Genomics of Cancer Unit, Molecular Oncology Division, San Raffaele Scientific Institute, Milan, Italy.
Claudio PassanantiInstitute of Molecular Biology and Pathology, CNR Department of Molecular Medicine "Sapienza" University, Rome, Italy.
Giovanni BlandinoTranslational Oncogenomic Laboratory, Molecular Medicine Area Regina Elena National Cancer Institute, Rome, Italy.
Maurizio FanciulliEpigenetics Laboratory, Molecular Medicine Area Regina Elena National Cancer Institute, Rome, Italy fanciulli@ifo.it.
National Cancer Institute · MYSapienza University of Rome · ITCineca · ITMayo Clinic in Arizona · USInstitute of Molecular Biology and Pathology · ITSan Raffaele University of Rome · ITUniversity of Milan · IT

Funding

Women's Cancer ProgramP30CA015083 · NCI · MAYO CLINIC ROCHESTER · PI Felicity Enders · 1985 to 2026
$151.3M
Project 4: Targeting Resistance to T-Cell Directed Therapy in Multiple MyelomaP50CA186781 · NCI · MAYO CLINIC ARIZONA · PI Rafael Fonseca · 2015 to 2026
$25.5M
PQD2 Rational Combination of Standard Agents and Immunotherapy to Treat MyelomaR01CA190045 · NCI · MAYO CLINIC ARIZONA · PI CHESI, MARTA · 2014 to 2017
$1.4M
NCI NIH HHS P30 CA015083NCI NIH HHS P50 CA186781NCI NIH HHS R01 CA190045
6 · The paper itself

Abstract

Mammalian target of rapamycin (mTOR) is a key protein kinase that regulates cell growth, metabolism, and autophagy to maintain cellular homeostasis. Its activity is inhibited by adverse conditions, including nutrient limitation, hypoxia, and DNA damage. In this study, we demonstrate that Che-1, a RNA polymerase II-binding protein activated by the DNA damage response, inhibits mTOR activity in response to stress conditions. We found that, under stress, Che-1 induces the expression of two important mTOR inhibitors, Redd1 and Deptor, and that this activity is required for sustaining stress-induced autophagy. Strikingly, Che-1 expression correlates with the progression of multiple myeloma and is required for cell growth and survival, a malignancy characterized by high autophagy response.

Indexed as

AnimalsApoptosis Regulatory ProteinsAutophagyCell Line, TumorCell SurvivalFemaleIntracellular Signaling Peptides and ProteinsMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2Mice, NudeMultiple MyelomaMultiprotein ComplexesPhosphorylationRepressor ProteinsStress, PhysiologicalTOR Serine-Threonine KinasesAATF protein, humanApoptosis Regulatory ProteinsDDIT4 protein, humanDEPTOR protein, humanIntracellular Signaling Peptides and ProteinsMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2MTOR protein, humanMultiprotein ComplexesRepressor ProteinsTOR Serine-Threonine KinasesTranscription FactorsautophagyChe‐1mTORmultiple myeloma

Identifiers

PMID25770584
PMCPMC4426481
OpenAlexW2001219687

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.