Evidence map›Paper›PMID 29204268›Full record

ReviewCell & bioscience2017

Role of metastasis-induced protein S100A4 in human non-tumor pathophysiologies.

Fei Fei, Jie Qu, Chunyuan Li, Xinlu Wang, Yuwei Li, Shiwu Zhang

Open access · goldAbstract readReview
In one paragraph

Review in Cell & bioscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

67 citing papers in PubMed, 110 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Non-Muscle Myosin II A: Friend or Foe in Cancer?International journal of molecular sciences · 2024
    Review
  18. Article
  19. Review
  20. Article

7 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Fei FeiNankai University School of Medicine, Nankai University, Tianjin, 300071 People's Republic of China.
Jie QuNankai University School of Medicine, Nankai University, Tianjin, 300071 People's Republic of China.
Chunyuan LiNankai University School of Medicine, Nankai University, Tianjin, 300071 People's Republic of China.
Xinlu WangDepartments of Pathology, Tianjin Union Medical Center, Tianjin, 300121 People's Republic of China.
Yuwei LiDepartments of Colorectal Surgery, Tianjin Union Medical Center, Tianjin, 300121 People's Republic of China.
Shiwu ZhangDepartments of Pathology, Tianjin Union Medical Center, Tianjin, 300121 People's Republic of China.
Nankai University · CNTianjin People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

S100A4, an important member of the S100 family of proteins, is best known for its significant role in promoting cancer progression and metastasis. In addition to its expression in tumors, upregulation of S100A4 expression has been associated with various non-tumor pathophysiology processes. However, the mechanisms underlying the role of S100A4 remain unclear. Activated "host" cells (fibroblasts, immunocytes, vascular cells, among others) secrete S100A4 into the extracellular space in various non-tumor human disorders, where it executes its biological functions by interacting with intracellular target proteins. However, the exact molecular mechanisms underlying these interactions in different non-tumor pathophysiologies vary, and S100A4 is likely one of the cross-linking factors that acts as common intrinsic constituents of biological mechanisms. Numerous studies have indicated that the S100A4-mediated epithelial-mesenchymal transition plays a vital role in the occurrence and development of various non-tumor pathophysiologies. Epithelial-mesenchymal transition can be categorized into three general subtypes based on the phenotype and function of the output cells. S100A4 regulates tissue fibrosis associated with the type II epithelial-mesenchymal transition via various signaling pathways. Additionally, S100A4 stimulates fibroblasts to secrete fibronectin and collagen, thus forming the structural components of the extracellular matrix (ECM) and stimulating their deposition in tissues, contributing to the formation of a pro-inflammatory niche. Simultaneously, S100A4 enhances the motility of macrophages, neutrophils, and leukocytes and promotes the recruitment and chemotaxis of these inflammatory cells to regulate inflammation and immune functions. S100A4 also exerts a neuroprotective pro-survival effect on neurons by rescuing them from brain injury and participates in angiogenesis by interacting with other target molecules. In this review, we summarize the role of S100A4 in fibrosis, inflammation, immune response, neuroprotection, angiogenesis, and some common non-tumor diseases as well as its possible involvement in molecular pathways and potential clinical value.

Indexed as

Epithelial–mesenchymal transitionFibrosisInflammationS100A4

Identifiers

PMID29204268
PMCPMC5702147
OpenAlexW2769160599

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.