Evidence map›Paper›PMID 27616044›Full record

ArticleScientific reports2016

ITF promotes migration of intestinal epithelial cells through crosstalk between the ERK and JAK/STAT3 pathways.

Juan Le, Duan Y Zhang, Yong Zhao, Wei Qiu, Peng Wang, Yong Sun

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
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  13. Trefoil Factor 3 (TFF3) Is Involved in Cell Migration for Skeletal Repair.International journal of molecular sciences · 2019
    Article
  14. Article
  15. Article
  16. Hypoxia-Induced Activation of JAK/STAT3 Signaling Pathway Promotes Trophoblast Cell Viability and Angiogenesis in Preeclampsia.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  17. Review
  18. 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

6 authors at 1 institution in 1 country.

Juan LeDepartment of Burn Surgery, Huaihai Hospital affiliated to Xuzhou Medical College, Xuzhou, Jiangsu Province, China.
Duan Y ZhangDepartment of Burn Surgery, Huaihai Hospital affiliated to Xuzhou Medical College, Xuzhou, Jiangsu Province, China.
Yong ZhaoDepartment of Burn Surgery, Huaihai Hospital affiliated to Xuzhou Medical College, Xuzhou, Jiangsu Province, China.
Wei QiuDepartment of Burn Surgery, Huaihai Hospital affiliated to Xuzhou Medical College, Xuzhou, Jiangsu Province, China.
Peng WangDepartment of Burn Surgery, Huaihai Hospital affiliated to Xuzhou Medical College, Xuzhou, Jiangsu Province, China.
Yong SunDepartment of Burn Surgery, Huaihai Hospital affiliated to Xuzhou Medical College, Xuzhou, Jiangsu Province, China.
Xuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intestinal trefoil factor (ITF), a member of the trefoil factor family, is a "Super-protective factor" for intestinal mucosal protection. This study was designed to explore the mechanism by which ITF promotes intestinal epithelial cell migration. Intestinal epithelial cells were treated with the human ITF (hITF). Phospho-ERK, phospho-STAT3 Tyr(705), and phospho-STAT3 Ser(727) levels were detected at different time points by western blot. To assess the potential crosstalk between the ERK and JAK/STAT3 pathways, HT-29 cells were treated with the MEK-inhibitor, U0126, and phosphor-STAT3 levels were evaluated. Conversely, cells were treated with the JAK-inhibitor, AG490, and ERK-activity was evaluated. Transwell assay was performed to investigate the effect of the crosstalk on the cell motility. MMP-2 and MMP-9 transcription was analyzed by quantitative real-time PCR. E-cadherin degradation was detected by immunofluorescence. Our results indicate that hITF simultaneously activated the ERK and JAK/STAT3 pathways and a crosstalk was detected between the two pathways. hITF increased cell migration. This effect was abolished by U0126 and AG490 treatment. hITF increased MMP2 and MMP9 mRNA levels and E-cadherin degradation and U0126 and AG490 abolished this effect of hITF. In conclusion, the hITF-induced crosstalk between the ERK and JAK/STAT3 pathways is associated with intestinal epithelial cell migration.

Indexed as

Antigens, CDButadienesCadherinsCell MovementEnzyme InhibitorsEpithelial CellsExtracellular Signal-Regulated MAP KinasesHEK293 CellsHT29 CellsHumansIntestinesJanus KinasesMatrix Metalloproteinase 2Matrix Metalloproteinase 9NitrilesSignal Transductionalpha-cyano-(3,4-dihydroxy)-N-benzylcinnamideAntigens, CDButadienesCadherinsCDH1 protein, humanEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesJanus KinasesMatrix Metalloproteinase 2Matrix Metalloproteinase 9MMP2 protein, humanMMP9 protein, humanNitrilesSTAT3 protein, humanSTAT3 Transcription FactorTFF3 protein, humanTrefoil Factor-3TyrphostinsU 0126

Identifiers

PMID27616044
PMCPMC5018822
OpenAlexW2519765664

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LicenceCC BY
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.