Evidence map›Paper›PMID 20383191›Full record

ArticleOncogene2010

CNK1 is a novel Akt interaction partner that promotes cell proliferation through the Akt-FoxO signalling axis.

R D Fritz, Z Varga, G Radziwill

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

16 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Turning off AKT: PHLPP as a drug target.Annual review of pharmacology and toxicology · 2014
    Review
  15. Article
  16. Dual mTORC2/mTORC1 targeting results in potent suppressive effects on acute myeloid leukemia (AML) progenitors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011
    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

3 authors at 3 institutions in 2 countries.

R D FritzInstitute of Medical Virology, University of Zurich, Zurich, Switzerland.
Z Varga
G Radziwill
University Hospital of Zurich · CHUniversity of Freiburg · DEUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The scaffold proteins connector enhancer of KSR (CNK) participate in Raf-, Rho- and NF-kappaB-dependent signalling and promote cell differentiation and invasion. In this study, we demonstrate that CNK1 downregulation inhibits, whereas CNK1 overexpression stimulates the proliferation of breast cancer cells and human embryonic kidney cells, respectively. This stimulatory effect depends on a functional phosphatidylinositol-3 kinase (PI3K) pathway because treatment of cells with the PI3K inhibitor, LY294002, abrogates CNK1-induced proliferation. CNK1 interacts with the PI3K effector Akt and knockdown of CNK1 decreases Akt activity in breast cancer cells. CNK1 controls Akt-dependent phosphorylation and transcriptional activity of FoxO, which is a negative regulator of proliferation. Consistent with this, CNK1-induced cell proliferation is blocked by FoxO overexpression. Moreover, CNK1 regulates anchorage-independent proliferation and focus formation of breast cancer cells. CNK1 is predominantly localized at the plasma membrane of breast cancer cells, whereas in non-transformed mammary epithelial cells, CNK1 is cytoplasmatic. Accordingly, CNK1 is found preferentially at the plasma membrane in carcinoma in situ and invasive breast cancer tumours compared with normal breast tissue sections. Analysis of multiple breast cancer samples reveals that CNK1-negative tumours show less Akt activity. Thus, CNK1 promotes oncogenic signalling through Akt in breast cancer cell lines and tumours.

Indexed as

Signal TransductionBreast NeoplasmsCell Line, TumorCell ProliferationForkhead Transcription FactorsGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsOncogenesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCNKSR1 protein, humanForkhead Transcription FactorsIntracellular Signaling Peptides and ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID20383191
OpenAlexW2050717486

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.