Evidence map›Paper›PMID 26487184›Full record

ArticleThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society2016

Enhanced Expression of Fibroblast Growth Factor Receptor 3 IIIc Promotes Human Esophageal Carcinoma Cell Proliferation.

Nobuhiro Ueno, Akio Shimizu, Michiyuki Kanai, Yugo Iwaya, Shugo Ueda, Jun Nakayama, Misuzu Kurokawa Seo

Open access · bronzeAbstract read
In one paragraph

Article in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 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
0.2field-weighted citation impact, top 43% 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, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Targeting the Microenvironment in Esophageal Cancer.Frontiers in cell and developmental biology · 2021
    Review
  7. Article
  8. Article
  9. Article
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 3 institutions in 1 country.

Nobuhiro UenoDepartment of Molecular Biosciences, Faculty of Life Sciences, Kyoto Sangyo University, Kyoto, Japan (NU, AS, MKS)
Akio ShimizuDepartment of Molecular Biosciences, Faculty of Life Sciences, Kyoto Sangyo University, Kyoto, Japan (NU, AS, MKS)
Michiyuki KanaiDigestive Disease Center, Hanwasumiyoshi General Hospital, Osaka, Japan (MK)
Yugo IwayaDepartment of Gastroenterology, Shinshu University School of Medicine, Matsumoto, Japan (YI)
Shugo UedaDepartment of Gastroenterological Surgery and Oncology, Kitano Hospital, Osaka, Japan (SU)
Jun NakayamaDepartment of Molecular Pathology, Shinshu University Graduate School of Medicine, Matsumoto, Japan (JN)
Misuzu Kurokawa SeoDepartment of Molecular Biosciences, Faculty of Life Sciences, Kyoto Sangyo University, Kyoto, Japan (NU, AS, MKS)
Kitano Hospital · JPShinshu University · JPKyoto Sangyo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deregulated expression of fibroblast growth factor receptors (FGFRs) and their ligands plays critical roles in tumorigenesis. The gene expression of an alternatively spliced isoforms of FGFR3, FGFR3IIIc, was analyzed by RT-PCR in samples from patients with esophageal carcinoma (EC), including esophageal squamous cell carcinoma (ESCC) and adenocarcinoma (EAC). The incidence of FGFR3IIIc was higher in EC [12/16 (75%); p=0.073] than in non-cancerous mucosa (NCM) [6/16 (38%)]. Indeed, an immunohistochemical analysis of early-stage ESCC showed that carcinoma cells expressing FGFR3IIIc stained positively with SCC-112, a tumor marker, and Ki67, a cell proliferation marker, suggesting that the expression of FGFR3IIIc promotes cell proliferation. We used EC-GI-10 cells endogenously expressing FGFR3IIIc as a model of ESCC to provide mechanistic insight into the role of FGFR3IIIc in ESCC. The knockdown of endogenous FGFR3 using siRNA treatment significantly abrogated cell proliferation and the overexpression of FGFR3IIIc in cells with enhanced cell proliferation. EC-GI-10 cells and ESCC from patients with EC showed endogenous expression of FGF2, a specific ligand for FGFR3IIIc, suggesting that the upregulated expression of FGFR3IIIc may create autocrine FGF signaling in ESCC. Taken together, FGFR3IIIc may have the potential to be an early-stage tumor marker and a molecular target for ESCC therapy.

Indexed as

AdenocarcinomaAgedCarcinoma, Squamous CellCell Line, TumorCell ProliferationEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaFemaleHEK293 CellsHumansMaleReceptor, Fibroblast Growth Factor, Type 3RNA, Small InterferingFGFR3 protein, humanReceptor, Fibroblast Growth Factor, Type 3RNA, Small Interferingbiological tumor markercell proliferationesophageal cancerfibroblast growth factor receptor 3molecular target therapy

Identifiers

PMID26487184
PMCPMC4810793
OpenAlexW2180193688

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.