Evidence map›Paper›PMID 25886367›Full record

ArticleBMC cancer2015

The involvement of insulin-like growth factor 2 binding protein 3 (IMP3) in pancreatic cancer cell migration, invasion, and adhesion.

Clarissa C Pasiliao, Che-Wei A Chang, Brent W Sutherland, Shannon M Valdez, David Schaeffer, Donald T Yapp, Sylvia S W Ng

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
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  4. iScience · 2023
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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

7 authors at 2 institutions in 1 country.

Clarissa C PasiliaoDepartment of Experimental Therapeutics, British Columbia Cancer Agency, 675 West 10th Avenue, Vancouver, BC, V5Z 1 L3, Canada. cpasiliao@gmail.com.
Che-Wei A ChangDepartment of Experimental Therapeutics, British Columbia Cancer Agency, 675 West 10th Avenue, Vancouver, BC, V5Z 1 L3, Canada. chewei68@hotmail.com.
Brent W SutherlandDepartment of Experimental Therapeutics, British Columbia Cancer Agency, 675 West 10th Avenue, Vancouver, BC, V5Z 1 L3, Canada. bsutherland@bccrc.ca.
Shannon M ValdezDepartment of Experimental Therapeutics, British Columbia Cancer Agency, 675 West 10th Avenue, Vancouver, BC, V5Z 1 L3, Canada. svaldez@bccrc.ca.
David SchaefferDepartment of Pathology and Laboratory Medicine, Faculty of Medicine, University of British Columbia, Vancouver, BC, V6T 2B5, Canada. david.schaeffer@vch.ca.
Donald T YappDepartment of Experimental Therapeutics, British Columbia Cancer Agency, 675 West 10th Avenue, Vancouver, BC, V5Z 1 L3, Canada. dyapp@bccrc.ca.
Sylvia S W NgDepartment of Experimental Therapeutics, British Columbia Cancer Agency, 675 West 10th Avenue, Vancouver, BC, V5Z 1 L3, Canada. sylvia.ng@rmp.uhn.ca.
BC Cancer Agency · CAUniversity of British Columbia · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

backgroundOver-expression of insulin-like growth factor 2 mRNA binding protein 3 (IMP3) is correlated with poor prognosis in pancreatic ductal adenocarcinoma (PDAC). Previous studies examining other cancer types have implicated IMP3 in the regulation of several cellular functions that are characteristic of tumour cells. However, the role of this oncofetal protein in PDAC progression remained unclear.

methodsUsing siRNA, we examined the effect of IMP3 inhibition on the motility, invasive ability, and matrix adhesion of PDAC cells. In addition, we also evaluated the expression of cytoskeleton-associated genes following IMP depletion.

resultsKnockdown of IMP3 significantly decreased the motility, invasion, and extracellular matrix adhesion of select PDAC cells in vitro. In addition, IMP3-depleted cells exhibited lower levels of CD44 protein and KIF11 mRNA. Moreover, we also observed a reduction in downstream RhoA signaling following IMP3 knockdown, indicating that IMP3 modulates the levels of proteins involved in cytoskeletal organization.

conclusionsThese results suggest that IMP3 facilitates PDAC progression by enhancing the pro-metastatic behaviour of tumour cells.

Indexed as

Biomarkers, TumorCarcinoma, Pancreatic DuctalCell AdhesionCell Line, TumorCell MovementGene Expression Regulation, NeoplasticGene Knockout TechniquesHumansNeoplasm InvasivenessNeoplasm MetastasisNeoplasm ProteinsRNA-Binding ProteinsRNA, MessengerBiomarkers, TumorIGF2BP3 protein, humanNeoplasm ProteinsRNA-Binding ProteinsRNA, Messenger

Identifiers

PMID25886367
PMCPMC4403680
OpenAlexW2084843340

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.