Evidence map›Paper›PMID 28892043›Full record

ArticleOncogene2018

Loss of PRP4K drives anoikis resistance in part by dysregulation of epidermal growth factor receptor endosomal trafficking.

D P Corkery, L E Clarke, S Gebremeskel, J Salsman, J Pinder, C Le Page, L Meunier, Z Xu, A-M Mes-Masson, J N Berman and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Yorkie/YAP Interactors: Fine-Tuning the Hippo Pathway Output.Cold Spring Harbor perspectives in biology · 2026
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  14. Haploinsufficient tumor suppressor PRP4K is negatively regulated during epithelial-to-mesenchymal transition.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
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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

12 authors at 2 institutions in 1 country.

D P CorkeryDepartment of Biochemistry & Molecular Biology, Dalhousie University, Halifax, Nova Scotia, Canada.
L E ClarkeDepartment of Pathology, Dalhousie University, Halifax, Nova Scotia, Canada.
S GebremeskelDepartment of Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia, Canada.
J SalsmanDepartment of Pathology, Dalhousie University, Halifax, Nova Scotia, Canada.
J PinderDepartment of Pathology, Dalhousie University, Halifax, Nova Scotia, Canada.
C Le PageCentre de recherche du Centre hospitalier de l'Université de Montréal (CRCHUM) and Institut du cancer de Montréal, Montreal, Quebec, Canada.
L MeunierCentre de recherche du Centre hospitalier de l'Université de Montréal (CRCHUM) and Institut du cancer de Montréal, Montreal, Quebec, Canada.
Z XuDepartment of Pathology, Dalhousie University, Halifax, Nova Scotia, Canada.
A-M Mes-MassonCentre de recherche du Centre hospitalier de l'Université de Montréal (CRCHUM) and Institut du cancer de Montréal, Montreal, Quebec, Canada.
J N BermanDepartment of Pathology, Dalhousie University, Halifax, Nova Scotia, Canada.
B JohnstonDepartment of Pathology, Dalhousie University, Halifax, Nova Scotia, Canada.
G DellaireDepartment of Biochemistry & Molecular Biology, Dalhousie University, Halifax, Nova Scotia, Canada.ORCID 0000-0002-3466-6316
Dalhousie University · CACentre Hospitalier de l’Université de Montréal · CA

Funding

CIHR MOP-110988CIHR PJT-153285
6 · The paper itself

Abstract

Anoikis acts as a critical barrier to metastasis by inducing cell death upon cancer cell detachment from the extracellular matrix (ECM), thereby preventing tumor cell dissemination to secondary sites. The induction of anoikis requires the lysosomal-mediated downregulation of epidermal growth factor receptors (EGFRs) leading to termination of pro-survival signaling. In this study, we demonstrate that depletion of pre-mRNA splicing factor 4 kinase (PRP4K; also known as PRPF4B) causes dysregulation of EGFR trafficking and anoikis resistance. We also report a novel cytoplasmic localization of PRP4K at the late endosome, and demonstrate both nuclear and cytoplasmic localization in breast, lung and ovarian cancer tissue. Mechanistically, depletion of PRP4K leads to reduced EGFR degradation following cell detachment from the ECM and correlates with increased TrkB, vimentin and Zeb1 expression. As a result, PRP4K loss promotes sustained growth factor signaling and increased cellular resistance to anoikis in vitro and in a novel zebrafish xenotransplantation model of anoikis sensitivity, as well as increased metastasis in a mouse model of ovarian cancer. Thus, PRP4K may serve as a potential biomarker of anoikis sensitivity in ovarian and other epithelial cancers.

Indexed as

AnimalsAnoikisBiomarkers, TumorBreast NeoplasmsCell Line, TumorCell NucleusDown-RegulationEndosomesEpidermal Growth FactorEpithelial CellsErbB ReceptorsFemaleHumansLung NeoplasmsMiceMice, Inbred C57BLBiomarkers, TumorEGFR protein, humanEpidermal Growth FactorErbB ReceptorsProtein Serine-Threonine KinasesPRPF4B protein, humanRibonucleoprotein, U4-U6 Small NuclearRNA, Small Interfering

Identifiers

PMID28892043
PMCPMC5770602
OpenAlexW2754128084

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.