Evidence map›Paper›PMID 24503018›Full record

ArticleEMBO molecular medicine2014

Nuclear translocation of FGFR1 and FGF2 in pancreatic stellate cells facilitates pancreatic cancer cell invasion.

Stacey J Coleman, Athina-Myrto Chioni, Mohammed Ghallab, Rhys K Anderson, Nicholas R Lemoine, Hemant M Kocher, Richard P Grose

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

92 citing papers in PubMed, 172 citations in OpenAlex.

  1. Blockade of FGFR1 Trafficking to the Cell Surface Results in the Partial Mistargeting of the Receptor to Peroxisomes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Mitochondrial double-stranded RNA fuels pancreatic cancer growth via RIG-I/TLR3 inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. FGF family in health and disease.Molecular biomedicine · 2026
    Review
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  10. Dual-Hit Strategy for Therapeutic Targeting of Pancreatic Cancer in Patient-Derived Xenograft Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  11. Fibroblast growth factor receptor 1 inhibition suppresses pancreatic cancer chemoresistance and chemotherapy-driven aggressiveness.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2024
    Article
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32 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Stacey J ColemanCentre for Tumour Biology Barts Cancer Institute - a CRUK Centre of Excellence, Queen Mary University of London, London, UK.
Athina-Myrto Chioni
Mohammed Ghallab
Rhys K Anderson
Nicholas R Lemoine
Hemant M Kocher
Richard P Grose
Queen Mary University of London · GBRoyal London Hospital · GB

Funding

Cancer Research UK 12008
6 · The paper itself

Abstract

Pancreatic cancer is characterised by desmoplasia, driven by activated pancreatic stellate cells (PSCs). Over-expression of FGFs and their receptors is a feature of pancreatic cancer and correlates with poor prognosis, but whether their expression impacts on PSCs is unclear. At the invasive front of human pancreatic cancer, FGF2 and FGFR1 localise to the nucleus in activated PSCs but not cancer cells. In vitro, inhibiting FGFR1 and FGF2 in PSCs, using RNAi or chemical inhibition, resulted in significantly reduced cell proliferation, which was not seen in cancer cells. In physiomimetic organotypic co-cultures, FGFR inhibition prevented PSC as well as cancer cell invasion. FGFR inhibition resulted in cytoplasmic localisation of FGFR1 and FGF2, in contrast to vehicle-treated conditions where PSCs with nuclear FGFR1 and FGF2 led cancer cells to invade the underlying extra-cellular matrix. Strikingly, abrogation of nuclear FGFR1 and FGF2 in PSCs abolished cancer cell invasion. These findings suggest a novel therapeutic approach, where preventing nuclear FGF/FGFR mediated proliferation and invasion in PSCs leads to disruption of the tumour microenvironment, preventing pancreatic cancer cell invasion.

Indexed as

Cell Line, TumorCell NucleusCell ProliferationFibroblast Growth Factor 2HumansNeoplasm InvasivenessPancreatic NeoplasmsPancreatic Stellate CellsProtein TransportReceptor, Fibroblast Growth Factor, Type 1Tumor MicroenvironmentFibroblast Growth Factor 2Receptor, Fibroblast Growth Factor, Type 1

Identifiers

PMID24503018
PMCPMC3992074
OpenAlexW2106968589

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.