Evidence map›Paper›PMID 24590173›Full record

ArticleThe Journal of cell biology2014

CIP2A oncoprotein controls cell growth and autophagy through mTORC1 activation.

Pietri Puustinen, Anna Rytter, Monika Mortensen, Pekka Kohonen, José M Moreira, Marja Jäättelä

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 2 pooled it
6.4field-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

50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 69 citations in OpenAlex.

  1. Guideline
  2. Guideline
  3. TransCONFIRM: Identification of a Genetic Signature of Response to Fulvestrant in Advanced Hormone Receptor-Positive Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Trial
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The Pivotal Role of Protein Phosphatase 2A (PP2A) in Brain Tumors.International journal of molecular sciences · 2022
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. CIP2A silencing alleviates doxorubicin resistance in MCF7/ADR cells through activating PP2A and autophagy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Article
  20. CIP2A regulates MYC translation (via its 5'UTR) in colorectal cancer.International journal of colorectal disease · 2021
    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

6 authors at 3 institutions in 3 countries.

Pietri PuustinenCell Death and Metabolism, Danish Cancer Society Research Center, 2100 Copenhagen, Denmark.
Anna Rytter
Monika Mortensen
Pekka Kohonen
José M Moreira
Marja Jäättelä
Danish Cancer Society · DKKarolinska Institutet · SEUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

mTORC1 (mammalian target of rapamycin complex 1) integrates information regarding availability of nutrients and energy to coordinate protein synthesis and autophagy. Using ribonucleic acid interference screens for autophagy-regulating phosphatases in human breast cancer cells, we identify CIP2A (cancerous inhibitor of PP2A [protein phosphatase 2A]) as a key modulator of mTORC1 and autophagy. CIP2A associates with mTORC1 and acts as an allosteric inhibitor of mTORC1-associated PP2A, thereby enhancing mTORC1-dependent growth signaling and inhibiting autophagy. This regulatory circuit is reversed by ubiquitination and p62/SQSTM1-dependent autophagic degradation of CIP2A and subsequent inhibition of mTORC1 activity. Consistent with CIP2A's reported ability to protect c-Myc against proteasome-mediated degradation, autophagic degradation of CIP2A upon mTORC1 inhibition leads to destabilization of c-Myc. These data characterize CIP2A as a distinct regulator of mTORC1 and reveals mTORC1-dependent control of CIP2A degradation as a mechanism that links mTORC1 activity with c-Myc stability to coordinate cellular metabolism, growth, and proliferation.

Indexed as

Cell ProliferationAutoantigensAutophagyCell Line, TumorComputational BiologyHumansIntracellular Signaling Peptides and ProteinsMechanistic Target of Rapamycin Complex 1Membrane ProteinsMultiprotein ComplexesProtein Phosphatase 2Proto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycRNA InterferenceRNA, Small InterferingSignal TransductionAutoantigensCIP2A protein, humanIntracellular Signaling Peptides and ProteinsMechanistic Target of Rapamycin Complex 1Membrane ProteinsMultiprotein ComplexesMYC protein, humanPPP2R3A protein, humanProtein Phosphatase 2Proto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycRNA, Small InterferingTOR Serine-Threonine Kinases

Identifiers

PMID24590173
PMCPMC3941044
OpenAlexW2132429277

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.