Evidence map›Paper›PMID 26743476›Full record

ArticleModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc2016

Inactivation of NKX6.3 in the stomach leads to abnormal expression of CDX2 and SOX2 required for gastric-to-intestinal transdifferentiation.

Jung H Yoon, Sung S Choi, Olga Kim, Won S Choi, Yong K Park, Suk W Nam, Jung Y Lee, Won S Park

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In one paragraph

Article in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed, 18 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Jung H YoonDepartment of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Sung S ChoiCollege of Pharmacy, Sahmyook University, Seoul, South Korea.
Olga KimDepartment of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Won S ChoiDepartment of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Yong K ParkDepartment of Biostatistics, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Suk W NamDepartment of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Jung Y LeeDepartment of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Won S ParkDepartment of Pathology, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
Catholic University of Korea · KRSahmyook University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intestinal metaplasia in gastric mucosa is considered a preneoplastic lesion that progresses to gastric cancer. However, the molecular networks underlying this lesion formation are largely unknown. NKX6.3 is known to be an important regulator in gastric mucosal epithelial differentiation. In this study, we characterized the effects of NKX6.3 that may contribute to gastric intestinal metaplasia. NKX6.3 expression was significantly reduced in gastric mucosae with intestinal metaplasia. The mRNA expression levels of both NKX6.3 and CDX2 predicted the intestinal metaplasia risk, with an area under the receiver operating characteristic curve value of 0.9414 and 0.9971, respectively. Notably, the NKX6.3 expression level was positively and inversely correlated with SOX2 and CDX2, respectively. In stable AGS(NKX6.3) and MKN1(NKX6.3) cells, NKX6.3 regulated the expression of CDX2 and SOX2 by directly binding to the promoter regions of both genes. Nuclear NKX6.3 expression was detected only in gastric epithelial cells without intestinal metaplasia. Furthermore, NKX6.3-induced TWSG1 bound to BMP4 and inhibited BMP4-binding activity to BMPR-II. These data suggest that NKX6.3 might function as a master regulator of gastric differentiation by affecting SOX2 and CDX2 expression and the NKX6.3 inactivation may result in intestinal metaplasia in gastric epithelial cells.

Indexed as

Cell TransdifferentiationGene SilencingAnimalsAntigens, BacterialArea Under CurveBacterial ProteinsBinding SitesBone Morphogenetic Protein 4CDX2 Transcription FactorCell Line, TumorCell Transformation, NeoplasticDisease Models, AnimalFemaleGastric MucosaGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseAntigens, BacterialBacterial ProteinsBMP4 protein, humanBone Morphogenetic Protein 4cagA protein, Helicobacter pyloriCDX2 protein, humanCDX2 Transcription FactorHomeodomain ProteinsNkx6-3 protein, humanProteinsRNA, MessengerSOX2 protein, humanSOXB1 Transcription FactorsTranscription FactorsTWSG1 protein, human

Identifiers

PMID26743476
OpenAlexW2257334411

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.