Evidence map›Paper›PMID 12439907›Full record

ArticleWorld journal of gastroenterology2002

Down-regulation of gut-enriched Kruppel-like factor expression in esophageal cancer.

Nan Wang, Zhi-Hua Liu, Fang Ding, Xiu-Qin Wang, Chuan-Nong Zhou, Min Wu

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

54 citing papers in PubMed, 78 citations in OpenAlex.

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  9. The Partial Role of KLF4 and KLF5 in Gastrointestinal Tumors.Gastroenterology research and practice · 2021
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  15. Involvement of CRF2 signaling in enterocyte differentiation.World journal of gastroenterology · 2017
    Article
  16. Krüppel-Like Factor 4 Enhances Sensitivity of Cisplatin to Esophageal Squamous Cell Carcinoma (ESCC) Cells.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  17. Article
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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

6 authors at 1 institution in 1 country.

Nan WangNational Laboratory of Molecular Oncology, Cancer Institute, Chinese Academy of Medical Sciences, Beijing 100021, China.
Zhi-Hua Liu
Fang Ding
Xiu-Qin Wang
Chuan-Nong Zhou
Min Wu
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimEsophageal carcinoma is one of the most common malignant tumors in China. But the molecular mechanisms of esophageal carcinoma remains unclear. Gut-enriched Kruppel-like factor (GKLF) is a newly identified transcription factor which is expressed abandantly in the epithelial cells of the gastrointestinal tract and deregulation of GKLF was linked to several types of cancer. It is of interest to study the expression and role of GKLF in esophageal carcinoma.

methodsSemi-quantitative RT-PCR was used to compare GKLF expression in esophageal squamous cell carcinoma to normal mucosa of the same patients. The serum deprivation inducibility of GKLF was observed in an esophageal squamous cancer cell line by comparison to the primary culture of human fibroblast. The effect of antisense GKLF transfection on the proliferation and adhesion of esophageal squamous cancer cell line was also observed.

resultsThe level of GKLF transcript is lower in esophageal squamous cell carcinoma compared to paired normal-appearing mucosa in 14 of 17 of the tumors analyzed. The serum deprivation inducibility of GKLF was greatly decreased in an esophageal squamous cancer cell line compared to the primary culture of human fibroblast. Decreased expression of GKLF in the esophageal cancer cell by antisense GKLF transfection increased its proliferation rate compared with that of vector transfected cell control (P<0.05). Transfection of antisense GKLF decreased its adhesion ability (P<0.05).

conclusionThe findings of this study demonstrate the down-regulation of GKLF in esophageal squamous cancer, and suggest that deregulation of GKLF may play a role in initiation and/or progression as well as the metastasis of esophageal squamous cancer.

Indexed as

AnimalsBase SequenceCarcinoma, Squamous CellCell AdhesionCell DivisionCells, CulturedCulture Media, Serum-FreeDNA-Binding ProteinsDNA, ComplementaryDNA, NeoplasmDown-RegulationEsophageal NeoplasmsFibroblastsHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsCulture Media, Serum-FreeDNA-Binding ProteinsDNA, ComplementaryDNA, NeoplasmKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsRNA, MessengerRNA, NeoplasmTranscription Factors

Identifiers

PMID12439907
PMCPMC4656400
OpenAlexW198233261

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.