Evidence map›Paper›PMID 27766744›Full record

ArticleClinical and translational science2016

PTTG1 Levels Are Predictive of Saracatinib Sensitivity in Ovarian Cancer Cell Lines.

I Nakachi, B A Helfrich, M A Spillman, E A Mickler, C J Olson, J L Rice, C D Coldren, L E Heasley, M W Geraci, R S Stearman

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

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  8. Genetic deletion of endothelial microRNA-15a/16-1 promotes cerebral angiogenesis and neurological recovery in ischemic stroke through Src signaling pathway.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
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  14. Targeting theOncotarget · 2017
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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

10 authors at 3 institutions in 1 country.

I NakachiDivision of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado Denver/Anschutz Medical Campus, Aurora, Colorado, USA.
B A HelfrichDivision of Medical Oncology, Department of Medicine, University of Colorado Denver/Anschutz Medical Campus, Aurora, Colorado, USA.
M A SpillmanDepartment of Obstetrics and Gynecology, University of Colorado Denver/Anschutz Medical Campus, Aurora, Colorado, USA.
E A MicklerDivision of Pulmonary Medicine, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA.
C J OlsonDivision of Pulmonary Medicine, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA.
J L RiceDivision of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado Denver/Anschutz Medical Campus, Aurora, Colorado, USA.
C D ColdrenPathGroup, Nashville, Tennessee, USA.
L E HeasleyDepartment of Craniofacial Biology, School of Dental Medicine, University of Colorado Denver/Anschutz Medical Campus, Aurora, Colorado, USA.
M W GeraciDivision of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado Denver/Anschutz Medical Campus, Aurora, Colorado, USA.
R S StearmanDivision of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado Denver/Anschutz Medical Campus, Aurora, Colorado, USA.
University of Colorado Denver · USUniversity of Colorado Anschutz Medical Campus · USIndiana University School of Medicine

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Src kinase is recognized as a key target for molecular cancer therapy. However, methods to efficiently select patients responsive to Src inhibitors are lacking. We explored the sensitivity of ovarian cancer cell lines to the Src kinase inhibitor saracatinib to identify predictive markers of drug sensitivity using gene microarrays. Pituitary tumor transforming gene 1 (PTTG1) was selected as a potential biomarker as mRNA levels were correlated with saracatinib resistance, as well as higher PTTG1 protein expression. PTTG1 expression was correlated with proliferation, cell division, and mitosis in ovarian cancer tissues data sets. In sensitive cell lines, saracatinib treatment decreased PTTG1 and fibroblast growth factor 2 (FGF2) protein levels. Downregulating PTTG1 by siRNAs increased saracatinib sensitivity in two resistant cell lines. Our results indicate PTTG1 may be a valuable biomarker in ovarian cancer to predict sensitivity to saracatinib, and could form the basis of a targeted prospective saracatinib trial for ovarian cancer.

Indexed as

BenzodioxolesCell Line, TumorCell ProliferationDown-RegulationDrug Resistance, NeoplasmFemaleFibroblast Growth Factor 2Gene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesGene SilencingHumansModels, BiologicalOvarian NeoplasmsPhosphorylationQuinazolinesBenzodioxolesFibroblast Growth Factor 2pituitary tumor-transforming protein 1, humanQuinazolinesRNA, MessengerRNA, Small InterferingsaracatinibSecurinsrc-Family Kinases

Identifiers

PMID27766744
PMCPMC5351005
OpenAlexW2533540020

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.