Evidence map›Paper›PMID 20046424›Full record

ArticleYonsei medical journal2009

Cyclooxygenase-2 expression is related to the epithelial-to-mesenchymal transition in human colon cancers.

Tae Jung Jang, Kyu Ha Jeon, Ki Hoon Jung

Open access · goldAbstract read
In one paragraph

Article in Yonsei medical journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.4field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 44 citations in OpenAlex.

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  7. Prostaglandin E2 accelerates invasion by upregulating Snail in hepatocellular carcinoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
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  13. Apricoxib, a novel inhibitor of COX-2, markedly improves standard therapy response in molecularly defined models of pancreatic cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012
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  17. Prostaglandins in cancer cell adhesion, migration, and invasion.International journal of cell biology · 2012
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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

3 authors at 1 institution in 1 country.

Tae Jung JangDepartment of Pathology, Dongguk University College of Medicine, Gyeongju, Korea. taejung@mail.dongguk.ac.kr
Kyu Ha Jeon
Ki Hoon Jung
Dongguk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeDown-regulation of E-cadherin is a hallmark of the epithelial-to-mesenchymal transition (EMT). EMT progression in cancer cells is associated with the loss of certain epithelial markers and the acquisition of a mesenchymal phenotype, as well as migratory activities. Cyclooxygenase-2 (COX-2) expression is associated with tumor invasion and metastasis in colon cancer. This study investigated the relationship between E-cadherin and COX-2 in colon cancer cells and human colon tumors. MATERIALS AND

methodsColon cancer cell lines and immunohistochemistry were used.

resultsE-cadherin expression was inversely related to the expressions of COX-2 and Snail in colon cancer cells. Ectopic expression of COX-2 or Snail reduced E-cadherin and induced a scattered, flattened phenotype with few intercellular contacts in colon cancer cells. Treatment of cancer cells with phorbol 12-myristate 13-acetate increased the expressions of COX-2 and Snail, decreased 15-hydroxyprostaglandin dehydrogenase expression, and increased the cells' motility. In addition, exposure to prostaglandin E(2) increased Snail expression and cell motility, and decreased E-cadherin expression. Membranous E-cadherin expression was lower in adenomas and cancers than in the adjacent, non-neoplastic epithelium. In contrast, the expressions of Snail and COX-2 were higher in cancers than in normal tissues and adenomas. The expressions of COX-2 and Snail increased in areas with abnormal E-cadherin expression. Moreover, COX-2 expression was related to higher tumor stages and was significantly higher in nodal metastatic lesions than primary cancers.

conclusionThis study suggests that COX-2 may have a role in tumor metastasis via EMT.

Indexed as

AdultAgedAged, 80 and overBlotting, WesternCadherinsCell DifferentiationCell Line, TumorCell MovementColonic NeoplasmsCyclooxygenase 2DinoprostoneEpithelial CellsEpitheliumFemaleHomeodomain ProteinsHT29 CellsCadherinsCyclooxygenase 2DinoprostoneHomeodomain ProteinsSnail Family Transcription FactorsTetradecanoylphorbol AcetateTranscription FactorsZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1colon cancersCOX-2E-cadherinEpithelial-to-mesenchymal transitionSnail

Identifiers

PMID20046424
PMCPMC2796410
OpenAlexW2116141371

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.