Evidence map›Paper›PMID 22945641›Full record

ArticleOncogene2013

β-Catenin signaling regulates Foxa2 expression during endometrial hyperplasia formation.

M Villacorte, K Suzuki, A Hirasawa, Y Ohkawa, M Suyama, T Maruyama, D Aoki, Y Ogino, S Miyagawa, T Terabayashi and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.9field-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

31 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Phospholipid flippase ATP11A brokers uterine epithelial integrity and function.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Sexually dimorphic effects of forkhead box a2 (FOXA2) and uterine glands on decidualization and fetoplacental development.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. Article
  13. Integrative analysis of the forkhead box A2 (FOXA2) cistrome for the human endometrium.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

13 authors at 8 institutions in 1 country.

M VillacorteDepartment of Developmental Genetics, Institute of Advanced Medicine, Wakayama Medical University, Wakayama, Kansai, Japan.
K Suzuki
A Hirasawa
Y Ohkawa
M Suyama
T Maruyama
D Aoki
Y Ogino
S Miyagawa
T Terabayashi
Y Tomooka
N Nakagata
G Yamada
Kumamoto University · JPKeio University · JPKyoto University · JPKyushu University · JPNational Institutes of Natural Sciences · JPOkazaki Institute for Integrative Bioscience · JPTokyo University of Science · JPWakayama Medical University · JP

Funding

EXTERNAL GENITALIA DEVELOPMENT AND HYPOSPADIASR01ES016597 · NIEHS · WASHINGTON UNIVERSITY · PI MA, LIANG · 2009 to 2013
$1.5M
NIEHS NIH HHS R01ES016597-01A1
6 · The paper itself

Abstract

The Wnt/β-catenin signaling is essential for various organogenesis and is often implicated during tumorigenesis. Dysregulated β-catenin signaling is associated with the formation of endometrial adenocarcinomas (EACs), which is considered as the common form of endometrial cancer in women. In the current study, we investigate the downstream target of Wnt/β-catenin signaling in the uterine epithelia and the mechanism leading to the formation of endometrial hyperplasia. We report that conditional ablation and activation of β-catenin in the uterine epithelia lead to aberrant epithelial structures and endometrial hyperplasia formation, respectively. We demonstrate that β-catenin regulates Foxa2 with its candidate upstream region for the uterine epithelia. Furthermore, knockdown of Foxa2 leads to defects in cell cycle regulation, suggesting a possible function of Foxa2 in the control of cell proliferation. We also observe that β-catenin and Foxa2 expression levels are augmented in the human specimens of complex atypical endometrial hyperplasia, which is considered to have a greater risk of progression to EACs. Thus, our study indicates that β-catenin regulates Foxa2 expression, and this interaction is possibly essential to control cell cycle progression during endometrial hyperplasia formation. Altogether, the augmented expression levels of β-catenin and Foxa2 are essential features during the formation of endometrial hyperplasia.

Indexed as

Animalsbeta CateninEndometrial HyperplasiaFemaleGene Expression RegulationGene Knockdown TechniquesHepatocyte Nuclear Factor 3-betaHumansImmunohistochemistryMiceOligonucleotide Array Sequence AnalysisSignal Transductionbeta CateninFOXA2 protein, humanFoxa2 protein, mouseHepatocyte Nuclear Factor 3-beta

Identifiers

PMID22945641
OpenAlexW2124743484

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.