Evidence map›Paper›PMID 35413817›Full record

ArticleBMC molecular and cell biology2022

COX-2 strengthens the effects of acid and bile salts on human esophageal cells and Barrett esophageal cells.

Shen Jiangang, Kang Nayoung, Wang Hongfang, Li Junda, Chen Li, Bai Xuefeng, Li Mingsong

Open access · goldAbstract read
In one paragraph

Article in BMC molecular and cell biology, 2022. 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
0.7field-weighted citation impact, top 33% 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, 3 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

7 authors at 5 institutions in 2 countries.

Shen JiangangGuangdong Provincial Key Laboratory of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Kang NayoungGuangdong Provincial Key Laboratory of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Wang HongfangDepartment of Gastroenterology, Shenzhen Luohu People' Hospital, Shenzhen, 518003, China.
Li JundaDepartment of Gastroenterology, Shenzhen Longhua District People' Hospital, Shenzhen, 518109, China.
Chen LiDepartment of Gastroenterology, Shenzhen Longhua District People' Hospital, Shenzhen, 518109, China.
Bai XuefengDepartment of Pathology and Comprehensive Cancer Center, Ohio State University Medical Centre, 129 Hamilton Hall, 1645 Neil Avenue, Columbus, OH, 43210, USA.
Li MingsongGuangdong Provincial Key Laboratory of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. lims661216@163.com.
Shenzhen Bao'an District People's Hospital · CNSouthern Medical University · CNNanfang Hospital · CNShenzhen Luohu People's Hospital · CNThe Ohio State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsInvestigate the effect and mechanism of COX-2 on viability, intestinal metaplasia, and atypia in human esophageal squamous and Barrett esophageal cell lines.

methodsHuman esophageal squamous and Barrett esophageal cell lines were transfected with a COX-2 expression vector and a COX-2 siRNA, and then were treated with acid, bile salts, and a mixture of both. Cell viability, the expression of COX-2, NF-κB(p65), CDX-2, MUC2, c-myb, and BMP-4, and the morphology and microstructure of cells were then observed.

resultsThe viability of COX-2 overexpressed cells was significantly higher than that of control cells, while the viability of COX-2 siRNA-treated cells was significantly lower than that of control cells. Intestinal metaplasia and atypia were observed in cells overexpressing COX-2. Acid, bile salts, and their mixture inhibited the viability of these two cell lines, but the inhibitory effect of the mixture was stronger than a single treatment in either. SiRNA mediated knockdown of COX-2 strengthened the antiproliferative effects of the mixture on HET-1A and BAR-T cells. The expression of p-p65, CDX-2, and BMP-4 was positively correlated with COX-2 expression, while the expression levels of p65, MUC2, and c-myb remained unchanged.

conclusionCOX-2 may influence the viability, atypia, and intestinal metaplasia of human esophageal cells and Barrett esophageal cells. Activation of the p-p65, CDX-2, and BMP-4 signaling pathways by COX-2 may be part of this mechanism.

Indexed as

Barrett EsophagusBile Acids and SaltsCyclooxygenase 2Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaCDX2 Transcription FactorHomeodomain ProteinsHumansMetaplasiaRNA, Small InterferingBile Acids and SaltsCDX2 Transcription FactorCyclooxygenase 2Homeodomain ProteinsPTGS2 protein, humanRNA, Small InterferingBarrett’s esophagusBone morphogenic protein-4Caudal-related homeobox transcription factor-2Cyclooxygenase-2Esophageal adenocarcinomaNuclear factor kappa B

Identifiers

PMID35413817
PMCPMC9004192
OpenAlexW4223545148

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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.