Evidence map›Paper›PMID 27677589›Full record

ArticleOncotarget2016

FGF4 induces epithelial-mesenchymal transition by inducing store-operated calcium entry in lung adenocarcinoma.

Lisha Qi, Wangzhao Song, Lingmei Li, Lu Cao, Yue Yu, Chunmin Song, Yalei Wang, Fei Zhang, Yang Li, Bin Zhang and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 50 citations in OpenAlex.

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  20. Differential engagement of ORAI1 and TRPC1 in the induction of vimentin expression by different stimuli.Laboratory investigation; a journal of technical methods and pathology · 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

11 authors at 3 institutions in 1 country.

Lisha QiDepartment of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China.
Wangzhao SongDepartment of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China.
Lingmei LiDepartment of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China.
Lu CaoDepartment of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China.
Yue YuDepartment of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China.
Chunmin SongDepartment of Family Planning, Maternity & Child Care Center of Luoyang, Luoyang 471000, China.
Yalei WangDepartment of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China.
Fei ZhangThe Key Laboratory of Tianjin Cancer Prevention and Treatment, Tianjin 300060, China.
Yang LiDepartment of Pancreatic Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China.
Bin ZhangDepartment of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China.
Wenfeng CaoDepartment of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China.
Tianjin Medical University Cancer Institute and Hospital · CNNational Clinical Research Center for Digestive Diseases · CNTianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several fibroblast growth factor (FGF) isoforms act to stimulate epithelial-mesenchymal transition (EMT) during cancer progression. FGF4 and FGF7 are two ligands of FGF receptor 2 (FGFR2). Using two lung adenocarcinoma (ADC) cell lines, A549 and H1299, we showed that FGF4, but not FGF7, altered cell morphology, promoted EMT-associated protein expression, and enhanced cell proliferation, migration/invasion and colony initiation. In addition, FGF4 increased store-operated calcium entry (SOCE) and expression of the calcium signal-associated protein Orai1. The SOCE inhibitor 2,5-di-tert-butylhydroquinone (BHQ) or Orai1 knockdown reversed all of the EMT-promoting effects of FGF4. BHQ also inhibited FGF4-induced EMT in a mouse xenograft model. Finally, 60 human lung ADC samples and 21 sets of matched specimens (primary and metastatic foci in lymph nodes from one patient) were used to confirm the clinicopathologic significance of FGF4 and its correlation with E-cadherin, Vimentin and Orai1 expression. Our study thus shows that FGF4 induces EMT by elevating SOCE in lung ADC.

Indexed as

Epithelial-Mesenchymal TransitionAdenocarcinomaAdenocarcinoma of LungAdultAgedAnimalsCadherinsCalciumCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalFemaleFibroblast Growth Factor 4Fibroblast Growth Factor 7Gene Knockdown TechniquesCadherinsCalciumFGF4 protein, humanFGF7 protein, humanFibroblast Growth Factor 4Fibroblast Growth Factor 7ORAI1 ProteinReceptor, Fibroblast Growth Factor, Type 2Vimentinepithelial-mesenchymal transitionFGF4FGF7Orai1store-operated calcium entry

Identifiers

PMID27677589
PMCPMC5342032
OpenAlexW2521580851

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.