Evidence map›Paper›PMID 27613835›Full record

ArticleOncotarget2016

Mechanism of suppressors of cytokine signaling 1 inhibition of epithelial-mesenchymal transition signaling through ROS regulation in colon cancer cells: suppression of Src leading to thioredoxin up-regulation.

Sung-Hoon Jung, Su-Min Kim, Choong-Eun Lee

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 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
1.7field-weighted citation impact, top 14% 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, 23 citations in OpenAlex.

  1. Classification based on tumor phenotypes enables the novel molecular characterization of esophagogastric junction cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2025
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  7. Inhibition of miR-155 Attenuates CD14Clinical, cosmetic and investigational dermatology · 2022
    Article
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  14. MiR-106a-5p promotes 5-FU resistance and the metastasis of colorectal cancer by targeting TGFβR2.International journal of clinical and experimental pathology · 2018
    Article
  15. Article
  16. 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

3 authors at 1 institution in 1 country.

Sung-Hoon JungDepartment of Biological Science, College of Science, Sungkyunkwan University, Suwon 440-746, Korea.
Su-Min KimDepartment of Biological Science, College of Science, Sungkyunkwan University, Suwon 440-746, Korea.
Choong-Eun LeeDepartment of Biological Science, College of Science, Sungkyunkwan University, Suwon 440-746, Korea.
Sungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reactive oxygen species (ROS) participate in malignant progression of cancers including epithelial-mesenchymal transition (EMT). We have investigated the role of suppressors of cytokine signaling (SOCS)1 as an inhibitor of ROS-induced EMT using colon cancer cell lines transduced with SOCS1 and shSOCS1. Hydrogen peroxide treatment induced EMT features such as elevation of vimentin and Snail with a corresponding reduction of E-cadherin. The EMT markers are significantly decreased upon SOCS1 over-expression while increased under SOCS1 knock-down. SOCS1 inhibited ROS signaling pathways associated with EMT such as Src, Jak, and p65. Of note, strong up-regulation of Src activity in SOCS1-ablated cells was responsible for the elevated signaling leading to EMT, as shSrc or Src inhibitor abolished the shSOCS1-induced promotion of EMT response. Suppression of ROS-inducible EMT markers and invasion in SOCS1 over-expressing cells correlated with significantly low intracellular ROS levels in these cells. Analysis of antioxidant enzymes in SOCS1-transduced cells revealed a selective up-regulation of thioredoxin (Trx1), while thioredoxin ablation restored ROS levels and the associated EMT markers. As a mechanism of thioredoxin up-regulation by SOCS1, inhibition of Src activity promoting nuclear translocation of Nrf-2 is proposed. Taken together, our data strongly indicate that SOCS1 antagonizes EMT by suppressing Src activity, leading to thioredoxin expression and down-regulation of ROS levels in colon cancer cells.

Indexed as

Epithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticActive Transport, Cell NucleusAntioxidantsCell Line, TumorColonic NeoplasmsDown-RegulationHCT116 CellsHumansHydrogen PeroxideNF-E2-Related Factor 2Reactive Oxygen SpeciesSignal TransductionSnail Family Transcription Factorssrc-Family KinasesSuppressor of Cytokine Signaling 1 ProteinAntioxidantsHydrogen PeroxideNFE2L2 protein, humanNF-E2-Related Factor 2Reactive Oxygen SpeciesSNAI1 protein, humanSnail Family Transcription FactorsSOCS1 protein, humansrc-Family KinasesSuppressor of Cytokine Signaling 1 ProteinThioredoxinsTXN protein, humanVimentinEMT signalingreactive oxygen speciesSrcsuppressors of cytokine signalingthioredoxin

Identifiers

PMID27613835
PMCPMC5308746
OpenAlexW2508438584

What OpenQuestion holds

Textmetadata
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.