Evidence map›Paper›PMID 16367903›Full record

ArticleCancer science2005

Differential expression of S100A2 and S100A4 in lung adenocarcinomas: clinicopathological significance, relationship to p53 and identification of their target genes.

Daisuke Matsubara, Toshiro Niki, Shumpei Ishikawa, Akiteru Goto, Etsuko Ohara, Takehiko Yokomizo, Claus W Heizmann, Hiroyuki Aburatani, Sachiko Moriyama, Hirokazu Moriyama and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer science, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.0field-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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Influence of S100A2 in Human Diseases.Diagnostics (Basel, Switzerland) · 2022
    Review
  4. Article
  5. Review
  6. Alterations in the CaExploration of targeted anti-tumor therapy · 2021
    Article
  7. Tumor-Suppressor p53TADChembiochem : a European journal of chemical biology · 2020
    Article
  8. Article
  9. Review
  10. Review
  11. S100A4 protects the myocardium against ischemic stress.Journal of molecular and cellular cardiology · 2016
    Article
  12. Article
  13. Article
  14. Altered gene expression in conjunctival squamous cell carcinoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2016
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

13 authors at 4 institutions in 2 countries.

Daisuke MatsubaraDepartment of Human Pathology, School of Medicine, The University of Tokyo, Tokyo, Japan.
Toshiro Niki
Shumpei Ishikawa
Akiteru Goto
Etsuko Ohara
Takehiko Yokomizo
Claus W Heizmann
Hiroyuki Aburatani
Sachiko Moriyama
Hirokazu Moriyama
Yoshihiro Nishimura
Nobuaki Funata
Masashi Fukayama
Tokyo Metropolitan Komagome Hospital · JPKumamoto University · JPThe University of Tokyo · JPUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies suggest that some S100 proteins are involved in the progression of certain types of cancer. However, no comprehensive data is currently available on the expression of S100 family genes in lung adenocarcinomas. Oligonucleotide array, quantitative reverse transcription-polymerase chain reaction and western blot analyses of lung adenocarcinoma cell lines and bronchiolar epithelial cells (SAEC and NHBE) revealed that S100A2 and S100A4 were the most strikingly downregulated and upregulated members of the S100 family, respectively. Immunohistochemical analyses of 94 primary lung adenocarcinomas showed that positive S100A2 expression (33/94, 35.1%) was significantly associated with lymphatic invasion (P=0.0233) and positive S100A4 expression (19/94, 20.2%) with vascular invasion (P=0.0454). Interestingly, a strong inverse relationship was found between S100A4 and p53 expression (P=0.0008). Survival analyses showed that S100A4 positivity was associated with poor patient prognosis (P=0.042). S100A2 positivity was not associated with patient survival when the whole patient group was analyzed; however, S100A2 positivity was a favorable prognostic indicator in patients with p53-negative tumors (P=0.0448). Finally, we used oligonucleotide array analyses and identified potential S100A2 and S100A4 target genes involved in cancer progression: S100A2 induced RUNX3 and REPRIMO; S100A4 induced EZRIN, RUNX1 and WISP1; S100A2 repressed EGFR, NFKB2 and RELA2; and S100A4 repressed ANXA10 and IL1RN. Thus, the present study demonstrates involvement of S100A2 and S100A4 in the progression of lung adenocarcinomas and an inverse association between S100A4 and p53 expression, and provides a list of targets regulated by S100A2 and S100A4.

Indexed as

Gene Expression Regulation, NeoplasticGenes, p53AdenocarcinomaAdultAgedAged, 80 and overBase SequenceBronchiCell LineCell Line, TumorChemotactic FactorsDNA PrimersFemaleHumansLung NeoplasmsMaleChemotactic FactorsDNA PrimersS100A2 protein, humanS100A4 protein, humanS100 Calcium-Binding Protein A4S100 Proteins

Identifiers

PMID16367903
PMCPMC11159992
OpenAlexW2086050575

What OpenQuestion holds

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Registered trials

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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.