Evidence map›Paper›PMID 30289335›Full record

ArticleAutophagy2019

Activated kinase screening identifies the

Margherita Leonardi, Eluisa Perna, Serena Tronnolone, David Colecchia, Mario Chiariello

Open access · hybridAbstract read
In one paragraph

Article in Autophagy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Cyclin-dependent kinases: Masters of the eukaryotic universe.Wiley interdisciplinary reviews. RNA · 2023
    Review
  11. Article
  12. Silencing IKBKE inhibits the migration and invasion of glioblastoma by promoting Snail1 degradation.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Article
  13. Article
  14. Article
  15. I-Oxidative medicine and cellular longevity · 2021
    Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review
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

5 authors at 2 institutions in 2 countries.

Margherita Leonardia Istituto per lo Studio, la Prevenzione e la Rete Oncologica (ISPRO) , Siena , Italy.ORCID 0000-0003-0148-170X
Eluisa Pernaa Istituto per lo Studio, la Prevenzione e la Rete Oncologica (ISPRO) , Siena , Italy.ORCID 0000-0002-5897-4671
Serena Tronnolonea Istituto per lo Studio, la Prevenzione e la Rete Oncologica (ISPRO) , Siena , Italy.ORCID 0000-0001-5524-1854
David Colecchiaa Istituto per lo Studio, la Prevenzione e la Rete Oncologica (ISPRO) , Siena , Italy.ORCID 0000-0002-0364-8924
Mario Chiarielloa Istituto per lo Studio, la Prevenzione e la Rete Oncologica (ISPRO) , Siena , Italy.ORCID 0000-0001-8434-5177
Istituto per lo Studio e la Prevenzione Oncologica · ITUniversity of Siena · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macroautophagy/autophagy is one of the major responses to stress in eukaryotic cells and is implicated in several pathological conditions such as infections, neurodegenerative diseases and cancer. Interestingly, cancer cells take full advantage of autophagy both to support tumor growth in adverse microenvironments and to oppose damages induced by anti-neoplastic therapies. Importantly, different human oncogenes are able to modulate this survival mechanism to support the transformation process, ultimately leading to 'autophagy addiction'. Still, oncogenic signaling events, impinging on the control of autophagy, are poorly characterized, limiting our possibilities to take advantage of these mechanisms for therapeutic purposes. Here, we screened a library of activated kinases for their ability to stimulate autophagy. By this approach, we identified novel potential regulators of the autophagic process and, among them, the IKBKE oncogene. Specifically, we demonstrate that this oncoprotein is able to stimulate autophagy when overexpressed, an event frequently found in breast tumors, and that its activity is strictly required for breast cancer cells to support the autophagic process. Interestingly, different oncogenic pathways typically involved in breast cancer, namely ERBB2 and PI3K-AKT-MTOR, also rely on IKBKE to control this process. Ultimately, we show that IKBKE-dependent autophagy is necessary for breast cancer cell proliferation, suggesting an important supporting role for this oncogene and autophagy in these tumors.

Indexed as

OncogenesAutophagyBiocatalysisCell Line, TumorCell Transformation, NeoplasticEnzyme ActivationEpithelial CellsErb-b2 Receptor Tyrosine KinasesFemaleHumansI-kappa B KinaseProtein KinasesSignal TransductionTriple Negative Breast NeoplasmsErb-b2 Receptor Tyrosine KinasesI-kappa B KinaseIKBKE protein, humanProtein KinasesAKTautophagybreast cancerIKBKEkinasessignal transduction

Identifiers

PMID30289335
PMCPMC6333447
OpenAlexW2895460376

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.