Evidence map›Paper›PMID 21177766›Full record

ArticleCarcinogenesis2011

P21-activated protein kinase (PAK2)-mediated c-Jun phosphorylation at 5 threonine sites promotes cell transformation.

Tingting Li, Jishuai Zhang, Feng Zhu, Weihong Wen, Tatyana Zykova, Xiang Li, Kangdong Liu, Cong Peng, Weiya Ma, Guozheng Shi and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 23% 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, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. JUNB and JUND in Urological Cancers: A Literature Review.Current issues in molecular biology · 2025
    Review
  5. Article
  6. Review
  7. Regulation of Cancer Metastasis by PAK2.International journal of molecular sciences · 2024
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Observational
  13. Article
  14. Article
  15. Article
  16. Expansion of BCR/ABL1British journal of haematology · 2017
    Article
  17. Article
  18. Article
  19. Article
  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

13 authors at 3 institutions in 2 countries.

Tingting LiThe Hormel Institute, University of Minnesota, 801 16th Avenue North East, Austin, MN 55912, USA.
Jishuai Zhang
Feng Zhu
Weihong Wen
Tatyana Zykova
Xiang Li
Kangdong Liu
Cong Peng
Weiya Ma
Guozheng Shi
Ziming Dong
Ann M Bode
Zigang Dong
Hormel (United States) · USUniversity of Minnesota · USZhengzhou University · CN

Funding

Anticarcinogenic Mechanisms of Tea ConstituentsR01CA081064 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI DONG, ZIGANG · 1999 to 2007
$1.9M
The role of histone phosphorylation in arsenic-induced cell transformation and skR01ES016548 · NIEHS · UNIVERSITY OF MINNESOTA · PI DONG, ZIGANG · 2008 to 2012
$1.7M
Anticarcinogenic Mechanisms of Tea ConstituentsR37CA081064 · NCI · UNIVERSITY OF MINNESOTA · PI DONG, ZIGANG · 2008 to 2012
$1.5M
Mechanisms of chemopreventive effect of resveratrolR01CA111536 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI DONG, ZIGANG · 2005 to 2009
$1.4M
Molecular basis of arsenic-induced cell transformationR01CA111356 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI DONG, ZIGANG · 2005 to 2007
$872k
NCI NIH HHS CA111356NCI NIH HHS CA111536NCI NIH HHS CA120588NCI NIH HHS R01 CA111356NCI NIH HHS R01 CA111536NCI NIH HHS R37 CA081064NCI NIH HHS R7CA081064NIEHS NIH HHS ES016548NIEHS NIH HHS R01 ES016548
6 · The paper itself

Abstract

The oncoprotein c-Jun is one of the components of the activator protein-1 (AP-1) transcription factor complex. AP-1 regulates the expression of many genes and is involved in a variety of biological functions such as cell transformation, proliferation, differentiation and apoptosis. AP-1 activates a variety of tumor-related genes and therefore promotes tumorigenesis and malignant transformation. Here, we found that epidermal growth factor (EGF) induces phosphorylation of c-Jun by P21-activated kinase (PAK) 2. Our data showed that PAK2 binds and phosphorylates c-Jun at five threonine sites (Thr2, Thr8, Thr89, Thr93 and Thr286) in vitro and ex vivo. Knockdown of PAK2 in JB6 Cl41 (P+) cells had no effect on c-Jun phosphorylation at Ser63 or Ser73 but resulted in decreases in EGF-induced anchorage-independent cell transformation, proliferation and AP-1 activity. Mutation at all five c-Jun threonine sites phosphorylated by PAK2 decreased the transforming ability of JB6 cells. Knockdown of PAK2 in SK-MEL-5 melanoma cells also decreased colony formation, proliferation and AP-1 activity. These results indicated that PAK2/c-Jun signaling plays an important role in EGF-induced cell proliferation and transformation.

Indexed as

AnimalsBlotting, WesternCell ProliferationCells, CulturedCell Transformation, NeoplasticEpidermal CellsEpidermal Growth FactorEpidermisHumansImmunoenzyme TechniquesImmunoprecipitationMelanomaMiceMutationp21-Activated KinasesPhosphorylationEpidermal Growth Factorp21-Activated KinasesProto-Oncogene Proteins c-junRNA, Small InterferingThreonineTranscription Factor AP-1

Identifiers

PMID21177766
PMCPMC3086698
OpenAlexW2096315226

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.