Evidence map›Paper›PMID 28288135›Full record

ArticleOncogene2017

Targeting Lyn regulates Snail family shuttling and inhibits metastasis.

D Thaper, S Vahid, K M Nip, I Moskalev, X Shan, S Frees, M E Roberts, K Ketola, K W Harder, C Gregory-Evans and 2 more

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

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  12. PAK5-stabilized Smuc confers renal cell carcinoma metastasis.Clinical and translational medicine · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

D ThaperDepartment of Urology, Vancouver Prostate Centre, University of British Columbia, Vancouver, BC, Canada.
S VahidDepartment of Urology, Vancouver Prostate Centre, University of British Columbia, Vancouver, BC, Canada.
K M NipDepartment of Urology, Vancouver Prostate Centre, University of British Columbia, Vancouver, BC, Canada.
I MoskalevDepartment of Urology, Vancouver Prostate Centre, University of British Columbia, Vancouver, BC, Canada.
X ShanFaculty of Medicine, Department Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, BC, Canada.
S FreesDepartment of Urology, Vancouver Prostate Centre, University of British Columbia, Vancouver, BC, Canada.
M E RobertsFaculty of Science, Department of Microbiology and Immunology, University of British Columbia, Vancouver, BC, Canada.
K KetolaDepartment of Urology, Vancouver Prostate Centre, University of British Columbia, Vancouver, BC, Canada.
K W HarderFaculty of Science, Department of Microbiology and Immunology, University of British Columbia, Vancouver, BC, Canada.
C Gregory-EvansFaculty of Medicine, Department Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, BC, Canada.
J L BishopDepartment of Urology, Vancouver Prostate Centre, University of British Columbia, Vancouver, BC, Canada.
A ZoubeidiDepartment of Urology, Vancouver Prostate Centre, University of British Columbia, Vancouver, BC, Canada.
University of British Columbia · CA

Funding

CIHR
6 · The paper itself

Abstract

The acquisition of an invasive phenotype by epithelial cells occurs through a loss of cellular adhesion and polarity, heralding a multistep process that leads to metastatic dissemination. Since its characterization in 1995, epithelial-mesenchymal transition (EMT) has been closely linked to the metastatic process. As a defining aspect of EMT, loss of cell adhesion through downregulation of E-cadherin is carried out by several transcriptional repressors; key among them the SNAI family of transcription factors. Here we identify for the first time that Lyn kinase functions as a key modulator of SNAI family protein localization and stability through control of the Vav-Rac1-PAK1 (Vav-Rac1-p21-activated kinase) pathway. Accordingly, targeting Lyn in vitro reduces EMT and in vivo reduces metastasis of primary tumors. We also demonstrate the clinical relevance of targeting Lyn as a key player controlling EMT; patient samples across many cancers revealed a strong negative correlation between Lyn and E-cadherin, and high Lyn expression in metastatic tumors as well as metastasis-prone primary tumors. This work reveals a novel pancancer mechanism of Lyn-dependent control of EMT and further underscores the role of this kinase in tumor progression.

Indexed as

AnimalsCell Line, TumorEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMiceMolecular Targeted TherapyNeoplasm MetastasisNeoplasmsProtein TransportRNA, Small InterferingSnail Family Transcription Factorssrc-Family KinasesXenograft Model Antitumor Assayslyn protein-tyrosine kinaseRNA, Small InterferingSnail Family Transcription Factorssrc-Family Kinases

Identifiers

PMID28288135
OpenAlexW2596341389

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.