Evidence map›Paper›PMID 22927998›Full record

ArticlePloS one2012

Gelsolin induces colorectal tumor cell invasion via modulation of the urokinase-type plasminogen activator cascade.

Jingli Zhuo, Ee Hong Tan, Benedict Yan, Lalchhandami Tochhawng, Manikandan Jayapal, Shiuan Koh, Hwee Kee Tay, Sutherland K Maciver, Shing Chuan Hooi, Manuel Salto-Tellez and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.1field-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

24 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
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  7. Susceptibility of cytoskeletal-associated proteins for tumor progression.Cellular and molecular life sciences : CMLS · 2021
    Review
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  12. Functional characterization of alternatively spliced GSN in head and neck squamous cell carcinoma.Translational research : the journal of laboratory and clinical medicine · 2018
    Article
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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

14 authors at 8 institutions in 5 countries.

Jingli ZhuoDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Ee Hong Tan
Benedict Yan
Lalchhandami Tochhawng
Manikandan Jayapal
Shiuan Koh
Hwee Kee Tay
Sutherland K Maciver
Shing Chuan Hooi
Manuel Salto-Tellez
Alan Prem Kumar
Yaw Chong Goh
Yaw Chyn Lim
Celestial T Yap
National University of Singapore · SGCancer Research UK Scotland Institute · GBCurtin University · AUKing Abdulaziz University · SANational University Hospital · SGSingapore General Hospital · SGUniversity of Edinburgh · GBUniversity of Glasgow · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gelsolin is a cytoskeletal protein which participates in actin filament dynamics and promotes cell motility and plasticity. Although initially regarded as a tumor suppressor, gelsolin expression in certain tumors correlates with poor prognosis and therapy-resistance. In vitro, gelsolin has anti-apoptotic and pro-migratory functions and is critical for invasion of some types of tumor cells. We found that gelsolin was highly expressed at tumor borders infiltrating into adjacent liver tissues, as examined by immunohistochemistry. Although gelsolin contributes to lamellipodia formation in migrating cells, the mechanisms by which it induces tumor invasion are unclear. Gelsolin's influence on the invasive activity of colorectal cancer cells was investigated using overexpression and small interfering RNA knockdown. We show that gelsolin is required for invasion of colorectal cancer cells through matrigel. Microarray analysis and quantitative PCR indicate that gelsolin overexpression induces the upregulation of invasion-promoting genes in colorectal cancer cells, including the matrix-degrading urokinase-type plasminogen activator (uPA). Conversely, gelsolin knockdown reduces uPA levels, as well as uPA secretion. The enhanced invasiveness of gelsolin-overexpressing cells was attenuated by treatment with function-blocking antibodies to either uPA or its receptor uPAR, indicating that uPA/uPAR activity is crucial for gelsolin-dependent invasion. In summary, our data reveals novel functions of gelsolin in colorectal tumor cell invasion through its modulation of the uPA/uPAR cascade, with potentially important roles in colorectal tumor dissemination to metastatic sites.

Indexed as

Signal TransductionCell Line, TumorColorectal NeoplasmsFibrinolysinGelsolinGene Expression Regulation, NeoplasticGene SilencingHumansNeoplasm InvasivenessReceptors, Urokinase Plasminogen ActivatorRNA, Small InterferingUrokinase-Type Plasminogen ActivatorFibrinolysinGelsolinReceptors, Urokinase Plasminogen ActivatorRNA, Small InterferingUrokinase-Type Plasminogen Activator

Identifiers

PMID22927998
PMCPMC3424201
OpenAlexW2149811051

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.