Evidence map›Paper›PMID 30267473›Full record

ArticleThoracic cancer2018

Blocking FGFR4 exerts distinct anti-tumorigenic effects in esophageal squamous cell carcinoma.

Zhongwei Xin, Xuemin Song, Bin Jiang, Xin Gongsun, Liang Song, Qiming Qin, Qiang Wang, Mo Shi, Xiangyan Liu

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 29% 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, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

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  17. Critical role of HOX transcript antisense intergenic RNA (HOTAIR) in gliomas.Journal of molecular medicine (Berlin, Germany) · 2020
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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

9 authors at 1 institution in 1 country.

Zhongwei XinDepartment of Thoracic Surgery, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong, China.
Xuemin SongDepartment of Thoracic Surgery, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong, China.
Bin JiangDepartment of Thoracic Surgery, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong, China.
Xin GongsunDepartment of Thoracic Surgery, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong, China.
Liang SongDepartment of Thoracic Surgery, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong, China.
Qiming QinDepartment of Thoracic Surgery, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong, China.
Qiang WangDepartment of Thoracic Surgery, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong, China.
Mo ShiDepartment of Thoracic Surgery, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong, China.
Xiangyan LiuDepartment of Thoracic Surgery, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong, China.ORCID 0000-0001-5118-2949
Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe FGFR family can be activated by FGFs and plays important roles in regulating cell growth, differentiation, migration, and angiogenesis. Recent studies have suggested that FGFR4 could regulate several processes, including tumor progression. Esophageal squamous cell carcinoma (ESCC) is a malignancy with high global occurrence. However, the molecule mechanism and the potential roles of FGFR4 in ESCC remain unknown.

methodsImmunohistochemistry and Western blotting were used to detect FGFR4 expression in ESCC samples and cell lines. Cell counting kit-8, and clonogenic, transwell, flow cytometric, and tumor xenograft in nude mice assays were utilized to determine the effect of blocking FGFR4 in proliferation, invasion, migration, and apoptosis of ESCC cells.

resultsFGFR4 is frequently overexpressed in ESCC tissue and cell lines. in vitro assays have shown that blocking FGFR4 by a specific blocker, H3B-6527, significantly decreases proliferation, invasion, and migration, and alters epithelial-mesenchymal transition markers in ESCC cells. In addition, FGFR4 blockade is associated with the induction of apoptosis and affects PI3K/Akt and MAPK/ERK pathways. Moreover, FGFR4 blockade could significantly inhibit the growth of xenograft tumors in vivo.

conclusionOur findings suggest that blocking FGFR4 significantly suppresses the malignant behaviors of ESCC and indicate that FGFR4 is a potential target for the treatment of ESCC.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalEpithelial-Mesenchymal TransitionEsophageal Squamous Cell CarcinomaGene ExpressionHumansImmunohistochemistryMiceNeoplasm StagingReceptor, Fibroblast Growth Factor, Type 4Antineoplastic AgentsFGFR4 protein, humanReceptor, Fibroblast Growth Factor, Type 4Epithelial-mesenchymal transition (EMT)esophageal squamous cell carcinoma (ESCC)FGFR4H3B-6527proliferation

Identifiers

PMID30267473
PMCPMC6275831
OpenAlexW2894106858

What OpenQuestion holds

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LicenceCC BY-NC
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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.