Evidence map›Paper›PMID 15111320›Full record

ArticleThe American journal of pathology2004

Beta-catenin simultaneously induces activation of the p53-p21WAF1 pathway and overexpression of cyclin D1 during squamous differentiation of endometrial carcinoma cells.

Makoto Saegusa, Miki Hashimura, Takeshi Kuwata, Mieko Hamano, Isao Okayasu

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. The tumor suppressor DLC1 inhibits cancer progression and oncogenic autophagy in hepatocellular carcinoma.Laboratory investigation; a journal of technical methods and pathology · 2018
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Epithelial to mesenchymal transition in the pathogenesis of uterine malignant mixed Müllerian tumours: the role of ubiquitin proteasome system and therapeutic opportunities.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2012
    Review
  17. Article
  18. Article
  19. Hypothesis: neoplasms in myotonic dystrophy.Cancer causes & control : CCC · 2009
    Review
  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

5 authors at 2 institutions in 1 country.

Makoto SaegusaDepartment of Pathology, Kitasato University School of Medicine, Kanagawa, Japan. msaegusa@med.kitasato-u.ac.jp
Miki Hashimura
Takeshi Kuwata
Mieko Hamano
Isao Okayasu
Kitasato University · JPJapanese Foundation For Cancer Research · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The functional consequences of up-regulation of beta-catenin as a transcription factor are complex in different tumors. To clarify roles during squamous differentiation (SqD) of endometrial carcinoma (Em Ca) cells, we investigated expression of beta-catenin, as well as cyclin D1, p53, p21WAF1, and PML (promyelocytic leukemia) in 80 cases of Em Ca with SqD areas, in comparison with cell proliferation determined with reference to Ki-67 antigen positivity. The impact of beta-catenin-T-cell factor (TCF)-mediated transcription was also examined using Em Ca cells. In clinical cases, nuclear beta-catenin accumulation was more frequent in SqD areas, being positively linked with expression of cyclin D1, p53, and p21WAF1, and inversely with Ki-67 and PML immunoreactivity. Significant correlations of nuclear beta-catenin, cyclin D1, p53, and p21WAF1 were noted between SqD and the surrounding carcinoma lesions. The Ishikawa cell line, with stable or tetracycline-regulated expression of mutant beta-catenin, showed an increase in expression levels of cyclin D1, p14ARF, p53, and p21WAF1 but not PML, and activation of beta-catenin-TCF4-mediated transcription determined with TOP/FOP constructs. The cell morphology was senescence-like rather than squamoid in appearance. Moreover, overexpressed beta-catenin could activate transcription from p14ARF and cyclin D1 promoters, in a TCF4-dependent manner. These findings indicate that in Em Cas, nuclear beta-catenin can simultaneously induce activation of the p53-p21WAF1 pathway and overexpression of cyclin D1, leading to suppression of cell proliferation or induction of cell senescence. However, overexpression of beta-catenin alone is not sufficient for development of a squamoid phenotype in Em Ca cells, suggesting that nuclear accumulation is an initial signal for trans-differentiation.

Indexed as

beta Cateninbeta-GalactosidaseBlotting, WesternCarcinoma, Squamous CellCell DifferentiationCell Line, TumorCell NucleusCellular SenescenceCyclin D1Cyclin-Dependent Kinase Inhibitor p21CyclinsCytoskeletal ProteinsEndometrial NeoplasmsEnzyme ActivationFemaleHumansbeta Cateninbeta-GalactosidaseCDKN1A protein, humanCTNNB1 protein, humanCyclin D1Cyclin-Dependent Kinase Inhibitor p21CyclinsCytoskeletal ProteinsKi-67 AntigenLuciferasesTrans-ActivatorsTumor Suppressor Protein p14ARFTumor Suppressor Protein p53

Identifiers

PMID15111320
PMCPMC1615666
OpenAlexW2055146852

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.