Evidence map›Paper›PMID 36411429›Full record

ArticleCell communication and signaling : CCS2022

PTEN overexpression and nuclear β-catenin stabilization promote morular differentiation through induction of epithelial-mesenchymal transition and cancer stem cell-like properties in endometrial carcinoma.

Ako Yokoi, Marina Minami, Miki Hashimura, Yasuko Oguri, Toshihide Matsumoto, Yoshinori Hasegawa, Mayu Nakagawa, Yu Ishibashi, Takashi Ito, Kensuke Ohhigata and 3 more

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Cell communication and signaling : CCS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. 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 2 institutions in 1 country.

Ako Yokoi *Department of Pathology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-Ku, Sagamihara, Kanagawa, 252-0374, Japan.
Marina Minami *Department of Pathology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-Ku, Sagamihara, Kanagawa, 252-0374, Japan.
Miki HashimuraDepartment of Pathology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-Ku, Sagamihara, Kanagawa, 252-0374, Japan.
Yasuko OguriDepartment of Pathology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-Ku, Sagamihara, Kanagawa, 252-0374, Japan.
Toshihide MatsumotoDepartment of Pathology, Kitasato University School of Allied Health Science, 1-15-1 Kitasato, Minami-Ku, Sagamihara, Kanagawa, 252-0374, Japan.
Yoshinori HasegawaLaboratory of Clinical Omics Research, Department of Applied Genomics, Kazusa DNA Research Institute, 2-6-7 Kazusakamatari, Kisarazu, Chiba, 292-0818, Japan.
Mayu NakagawaDepartment of Pathology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-Ku, Sagamihara, Kanagawa, 252-0374, Japan.
Yu IshibashiDepartment of Pathology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-Ku, Sagamihara, Kanagawa, 252-0374, Japan.
Takashi ItoDepartment of Pathology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-Ku, Sagamihara, Kanagawa, 252-0374, Japan.
Kensuke OhhigataDepartment of Pathology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-Ku, Sagamihara, Kanagawa, 252-0374, Japan.
Youhei HaradaDepartment of Pathology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-Ku, Sagamihara, Kanagawa, 252-0374, Japan.
Naomi FukagawaDepartment of Pathology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-Ku, Sagamihara, Kanagawa, 252-0374, Japan.
Makoto SaegusaDepartment of Pathology, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-Ku, Sagamihara, Kanagawa, 252-0374, Japan. msaegusa@med.kitasato-u.ac.jp.
Kitasato University · JPKazusa DNA Research Institute · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough a lack of functional PTEN contributes to tumorigenesis in a wide spectrum of human malignancies, little is known about the functional role of its overexpression in the tumors. The current study focused on PTEN overexpression in endometrial carcinoma (Em Ca).

methodsThe functional impact of PTEN overexpression was assessed by Em Ca cell lines. Immunohistochemical analyses were also conducted using 38 Em Ca with morular lesions.

resultsEm Ca cell lines stably overexpressing PTEN (H6-PTEN) exhibited epithelial-mesenchymal transition (EMT)-like features, probably through β-catenin/Slug-meditated suppression of E-cadherin. PTEN overexpression also inhibited cell proliferation, accelerated cellular senescence, increased apoptotic features, and enhanced migration capability. Moreover, H6-PTEN cells exhibited cancer stem cell (CSC)-like properties, along with high expression of aldehyde dehydrogenase 1 and CD44s, a large ALDH 1

conclusionIn the abscess of ERα/EBP50 expression, PTEN overexpression and nuclear β-catenin stabilization promote the establishment and maintenance of morular phenotype associated with EMT/CSC-like features in Em Ca cells. Video Abstract.

Indexed as

Endometrial NeoplasmsPTEN PhosphohydrolaseAnimalsbeta CateninEpithelial-Mesenchymal TransitionEstrogen Receptor alphaFemaleHumansNeoplastic Stem Cellsbeta CateninEstrogen Receptor alphaPTEN PhosphohydrolasePTEN protein, humanCancer stem cellEBP50Endometrial carcinomaMorulePTENβ-catenin

Identifiers

PMID36411429
PMCPMC9677676
OpenAlexW4309657301

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.