Evidence map›Paper›PMID 25772234›Full record

ArticleOncogene2016

DUSP10 regulates intestinal epithelial cell growth and colorectal tumorigenesis.

C W Png, M Weerasooriya, J Guo, S J James, H M Poh, M Osato, R A Flavell, C Dong, H Yang, Y Zhang

Abstract 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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. How metabolism bridles cytotoxic CD8Trends in immunology · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. PAC1-ing up the epigenetic landscape.Nature immunology · 2020
    Article
  17. Article
  18. Article
  19. Review
  20. Observational
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 4 institutions in 3 countries.

C W PngDepartment of Microbiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
M WeerasooriyaDepartment of Microbiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
J GuoCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
S J JamesDepartment of Microbiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
H M PohDepartment of Microbiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
M OsatoCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
R A FlavellDepartment of Immunology, Howard Hughes Medical Institute, Yale University, New Haven, CT, USA.
C DongDepartment of Basic Medical Sciences, Tsinghua University School of Medicine, Beijing, China.
H YangCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Y ZhangDepartment of Microbiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
National University of Singapore · SGHoward Hughes Medical Institute · USNational University Cancer Institute, Singapore · SGTsinghua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dual specificity phosphatase 10 (DUSP10), also known as MAP kinase phosphatase 5 (MKP5), negatively regulates the activation of MAP kinases. Genetic polymorphisms and aberrant expression of this gene are associated with colorectal cancer (CRC) in humans. However, the role of DUSP10 in intestinal epithelial tumorigenesis is not clear. Here, we showed that DUSP10 knockout (KO) mice had increased intestinal epithelial cell (IEC) proliferation and migration and developed less severe colitis than wild-type (WT) mice in response to dextran sodium sulphate (DSS) treatment, which is associated with increased ERK1/2 activation and Krüppel-like factor 5 (KLF5) expression in IEC. In line with increased IEC proliferation, DUSP10 KO mice developed more colon tumours with increased severity compared with WT mice in response to administration of DSS and azoxymethane (AOM). Furthermore, survival analysis of CRC patients demonstrated that high DUSP10 expression in tumours was associated with significant improvement in survival probability. Overexpression of DUSP10 in Caco-2 and RCM-1 cells inhibited cell proliferation. Our study showed that DUSP10 negatively regulates IEC growth and acts as a suppressor for CRC. Therefore, it could be targeted for the development of therapies for colitis and CRC.

Indexed as

AnimalsCaco-2 CellsCell ProliferationColitisColorectal NeoplasmsDextran SulfateDual-Specificity PhosphatasesEpithelial CellsExtracellular Signal-Regulated MAP KinasesGenes, Tumor SuppressorHumansIntestinesKruppel-Like Transcription FactorsMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase PhosphatasesDextran SulfateDual-Specificity PhosphatasesDUSP10 protein, humanDusp10 protein, mouseExtracellular Signal-Regulated MAP KinasesKlf5 protein, mouseKruppel-Like Transcription FactorsMitogen-Activated Protein Kinase Phosphatases

Identifiers

PMID25772234
OpenAlexW2052806541

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.