Evidence map›Paper›PMID 38146657›Full record

ArticleCell cycle (Georgetown, Tex.)2023

CXADR promote epithelial-mesenchymal transition in endometriosis by modulating AKT/GSK-3β signaling.

Hang-Jing Tan, Zi-Heng Deng, Chun Zhang, Hong-Wen Deng, Hong-Mei Xiao

Open access · greenAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

0 citing papers in PubMed, 5 citations in OpenAlex.

No citing paper in PubMed yet.

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 3 institutions in 2 countries.

Hang-Jing TanInstitute of Reproduction and Stem Cell Engineering, School of Basic Medical Science, Central South University, Changsha, China.
Zi-Heng DengInstitute of Reproduction and Stem Cell Engineering, School of Basic Medical Science, Central South University, Changsha, China.
Chun ZhangDepartment of Gynaecology and Obstetrics, Xiangya Hospital, Central South University, Changsha, China.
Hong-Wen DengCenter of Biomedical Informatics and Genomics, Deming Department of Medicine, Tulane University School of Medicine, New Orleans, LA, USA.
Hong-Mei XiaoInstitute of Reproduction and Stem Cell Engineering, School of Basic Medical Science, Central South University, Changsha, China.
Central South University · CNTulane University · USXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometriosis is a benign high prevalent disease exhibiting malignant features. However, the underlying pathogenesis and key molecules of endometriosis remain unclear. By integrating and analysis of existing expression profile datasets, we identified coxsackie and adenovirus receptor (CXADR), as a novel key gene in endometriosis. Based on the results of immunohistochemistry (IHC), we confirmed significant down-regulation of CXADR in ectopic endometrial tissues obtained from women with endometriosis compared with healthy controls. Further

Indexed as

EndometriosisProto-Oncogene Proteins c-aktCell Adhesion MoleculesCell Line, TumorCell MovementCoxsackie and Adenovirus Receptor-Like Membrane ProteinEpithelial-Mesenchymal TransitionFemaleGlycogen Synthase Kinase 3 betaHumansPhosphoprotein PhosphatasesPhosphoric Monoester HydrolasesSnail Family Transcription FactorsCell Adhesion MoleculesCLMP protein, humanCoxsackie and Adenovirus Receptor-Like Membrane ProteinGlycogen Synthase Kinase 3 betaPHLPP2 protein, humanPhosphoprotein PhosphatasesPhosphoric Monoester HydrolasesProto-Oncogene Proteins c-aktSnail Family Transcription FactorsAKT-signaling pathwayCXADR, EMTEndometriosis

Identifiers

PMID38146657
PMCPMC10802198
OpenAlexW4390231211

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.