Evidence map›Paper›PMID 34479599›Full record

ReviewCell communication and signaling : CCS2021

TLR4 signaling in the development of colitis-associated cancer and its possible interplay with microRNA-155.

Jie Guo, Mengfan Liao, Jun Wang

Open access · goldAbstract readReview
In one paragraph

Review in Cell communication and signaling : CCS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Article
  3. International journal of molecular sciences · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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.

Jie GuoHubei Province Key Laboratory of Occupational Hazard Identification and Control, Wuhan University of Science and Technology, Wuhan, China.
Mengfan LiaoHubei Province Key Laboratory of Occupational Hazard Identification and Control, Wuhan University of Science and Technology, Wuhan, China.
Jun WangHubei Province Key Laboratory of Occupational Hazard Identification and Control, Wuhan University of Science and Technology, Wuhan, China. wangjun@wust.edu.cn.ORCID 0000-0002-1679-1922
Wuhan University of Science and Technology · CN

Funding

National Natural Science Foundation of China (CN) 81602108National Natural Science Funding of China 71974153
6 · The paper itself

Abstract

Ulcerative colitis (UC) has closely been associated with an increased risk of colorectal cancer. However, the exact mechanisms underlying colitis-associated cancer (CAC) development remain unclear. As a classic pattern-recognition receptor, Toll like receptor (TLR)4 is a canonical receptor for lipopolysaccharide of Gram-negative bacteria (including two CAC-associated pathogens Fusobacterium nucleatum and Salmonella), and functions as a key bridge molecule linking oncogenic infection to colonic inflammatory and malignant processes. Accumulating studies verified the overexpression of TLR4 in colitis and CAC, and the over-expressed TLR4 might promote colitis-associated tumorigenesis via facilitating cell proliferation, protecting malignant cells against apoptosis, accelerating invasion and metastasis, as well as contributing to the creation of tumor-favouring cellular microenvironment. In recent years, considerable attention has been focused on the regulation of TLR4 signaling in the context of colitis-associated tumorigenesis. MicroRNA (miR)-155 and TLR4 exhibited a similar dynamic expression change during CAC development and shared similar CAC-promoting properties. The available data demonstrated an interplay between TLR4 and miR-155 in the context of different disorders or cell lines. miR-155 could augment TLR4 signaling through targeting negative regulators SOCS1 and SHIP1; and TLR4 activation would induce miR-155 expression via transcriptional and post-transcriptional mechanisms. This possible TLR4-miR-155 positive feedback loop might result in the synergistic accelerating effect of TLR4 and miR-155 on CAC development. Video abstract.

Indexed as

CarcinogenesisCell ProliferationColitis-Associated NeoplasmsGene Expression Regulation, NeoplasticHumansMicroRNAsPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesSignal TransductionSuppressor of Cytokine Signaling 1 ProteinToll-Like Receptor 4Tumor MicroenvironmentINPP5D protein, humanMicroRNAsMIRN155 microRNA, humanPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesSOCS1 protein, humanSuppressor of Cytokine Signaling 1 ProteinTLR4 protein, humanToll-Like Receptor 4Colitis-associated cancerInflammatory bowel diseaseMicroRNA-155Positive feedback loopToll like receptor 4

Identifiers

PMID34479599
PMCPMC8414775
OpenAlexW3196604154

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.