Evidence map›Paper›PMID 17653079›Full record

ArticleOncogene2008

CEACAM5 and CEACAM6 are major target genes for Smad3-mediated TGF-beta signaling.

S-U Han, T-H Kwak, K H Her, Y-H Cho, C Choi, H-J Lee, S Hong, Y S Park, Y-S Kim, T-A Kim and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

43 citing papers in PubMed, 63 citations in OpenAlex.

  1. CEACAM5 drives psoriatic inflammation by regulating CD8Biochemistry and biophysics reports · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. The emerging roles of CEACAM6 in human cancer (Review).International journal of oncology · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Frontiers in oncology · 2022
    Article
  18. Regulation of CEACAM5 and Therapeutic Efficacy of an Anti-CEACAM5-SN38 Antibody-drug Conjugate in Neuroendocrine Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
    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

11 authors at 4 institutions in 2 countries.

S-U HanLaboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
T-H Kwak
K H Her
Y-H Cho
C Choi
H-J Lee
S Hong
Y S Park
Y-S Kim
T-A Kim
S-J Kim
National Cancer Institute · USNational Institutes of Health · USHanyang University · KRKorea Research Institute of Bioscience and Biotechnology · KR

Funding

Intramural NIH HHS
6 · The paper itself

Abstract

The carcinoembryonic antigen (CEAs) family consists of a large group of evolutionarily and structurally divergent glycoproteins. The transforming growth factor-beta (TGF-beta) signaling pathway has been implicated in the stimulation of CEA secretion in TGF-beta-sensitive colon cells, thereby possibly modulating cell adhesion and differentiation. However, the specific CEAs targeted by TGF-beta signaling or underlying mechanism of the expression of CEAs has not yet been clarified. In this study, we investigated the specific CEAs targeted by the TGF-beta signaling pathway. In nine human gastric cancer cell lines examined, TGF-beta-responsive cell lines showed positive expression of CEAs. Expression patterns of CEA proteins correlated well with the level of CEA (CEACAM5) and CEACAM6 transcripts in these cell lines, but CEACAM1 expression was not observed in all of these cells. To investigate the role of TGF-beta signaling in CEA expression, we selected two TGF-beta unresponsive gastric cancer cell lines; SNU638 cells that contain a mutation in the TGF-beta type II receptor and SNU484 cells that express low to undetectable level of the TGF-beta pathway intermediate protein, Smad3. Restoration of TGF-beta signaling in these cells induced expression of the CEAs and increased activity of both CEA (CEACAM5) and CEACAM6 promoters. CEA expression was observed in the epithelium of the stomach of wild-type mice, but was markedly decreased in Smad3 null mice. These findings suggest that CEA (CEACAM5) and CEACAM6 are major target genes for Smad3-mediated TGF-beta signaling.

Indexed as

AnimalsAntigens, CDCarcinoembryonic AntigenCell Adhesion MoleculesCell Line, TumorGPI-Linked ProteinsHumansMiceProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IISmad3 ProteinStomach NeoplasmsTransforming Growth Factor betaAntigens, CDCarcinoembryonic AntigenCD66 antigensCEACAM5 protein, humanCEACAM6 protein, humanCell Adhesion MoleculesGPI-Linked ProteinsProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IISmad3 ProteinSMAD3 protein, humanTransforming Growth Factor beta

Identifiers

PMID17653079
OpenAlexW2066594663

What OpenQuestion holds

Textmetadata
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.