Evidence map›Paper›PMID 25961922›Full record

ArticleOncogene2016

p38γ MAPK is required for inflammation-associated colon tumorigenesis.

N Yin, X Qi, S Tsai, Y Lu, Z Basir, K Oshima, J P Thomas, C R Myers, G Stoner, G Chen

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

35 citing papers in PubMed, 43 citations in OpenAlex.

  1. p38γ and p38δ MAP kinases in inflammation.Biochemical Society transactions · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. A retrospective analysis of the clinicopathological features and prognostic value of MAPK12 protein expression in diffuse large B-cell lymphoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. P38 kinase in gastrointestinal cancers.Cancer gene therapy · 2023
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. The Hallmarks of Flavonoids in Cancer.Molecules (Basel, Switzerland) · 2021
    Review
  19. Article
  20. The Role of p38γ in Cancer: From review to outlook.International journal of biological sciences · 2021
    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

10 authors at 1 institution in 1 country.

N YinDepartment of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, MI, USA.
X QiDepartment of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, MI, USA.
S TsaiDepartment of Surgery, Medical College of Wisconsin, Milwaukee, MI, USA.
Y LuDepartment of Physiology, Medical College of Wisconsin, Milwaukee, MI, USA.
Z BasirDepartment of Pathology, Medical College of Wisconsin, Milwaukee, MI, USA.
K OshimaDepartment of Pathology, Medical College of Wisconsin, Milwaukee, MI, USA.
J P ThomasDepartment of Medicine, Medical College of Wisconsin, Milwaukee, MI, USA.
C R MyersDepartment of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, MI, USA.
G StonerDepartment of Medicine, Medical College of Wisconsin, Milwaukee, MI, USA.
G ChenDepartment of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, MI, USA.
Medical College of Wisconsin · US

Funding

A protein-complex as a novel therapeutic target for K-Ras dependent colon cancerI01BX002883 · VA · CLEMENT J. ZABLOCKI VA MEDICAL CENTER · PI CHEN, GUAN · 2015 to 2018
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BLRD VA I01 BX002883
6 · The paper itself

Abstract

Chronic inflammation has long been considered to causatively link to colon cancer development. However, signal transduction pathways involved remain largely unidentified. Here, we report that p38γ mitogen-activated protein kinase mediates inflammatory signaling to promote colon tumorigenesis. Inflammation activates p38γ in mouse colon tissues and intestinal epithelial cell-specific p38γ knockout (KO) attenuates colitis and inhibits pro-inflammatory cytokine expression. Significantly, p38γ KO inhibits tumorigenesis in a colitis-associated mouse model. The specific p38γ pharmacological inhibitor pirfenidone also suppresses pro-inflammatory cytokine expression and colon tumorigenesis. The tumor-promoting activity of epithelial p38γ was further demonstrated by xenograft studies. In addition, p38γ is required for β-catenin/Wnt activities and p38γ stimulates Wnt transcription by phosphorylating β-catenin at Ser605. These results show that p38γ activation links inflammation and colon tumorigenesis. Targeting p38γ may be a novel strategy for colon cancer prevention and treatment.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalCarcinogenesisColonic NeoplasmsCytokinesEnzyme ActivationHumansInflammationMiceMice, Inbred C57BLMice, KnockoutMice, NudeMitogen-Activated Protein Kinase 12Neoplasm TransplantationPyridonesSignal TransductionAnti-Inflammatory Agents, Non-SteroidalCytokinesMitogen-Activated Protein Kinase 12pirfenidonePyridones

Identifiers

PMID25961922
OpenAlexW796430143

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.