Evidence map›Paper›PMID 26777065›Full record

ArticleScientific reports2016

Squalene epoxidase is a bona fide oncogene by amplification with clinical relevance in breast cancer.

David N Brown, Irene Caffa, Gabriella Cirmena, Daniela Piras, Anna Garuti, Maurizio Gallo, Saverio Alberti, Alessio Nencioni, Alberto Ballestrero, Gabriele Zoppoli

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

95 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.

  1. Squalene Epoxidase: Its Regulations and Links with Cancers.International journal of molecular sciences · 2024
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35 more citing papers are in PubMed but not listed here.

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 4 institutions in 2 countries.

David N BrownJ.-C. Heuson Breast Cancer Translational Research Laboratory, Institut Jules Bordet, Brussels BE.
Irene CaffaDepartment of Internal Medicine (Di.M.I.), University of Genova, Genova IT.
Gabriella CirmenaDepartment of Internal Medicine (Di.M.I.), University of Genova, Genova IT.
Daniela PirasDepartment of Internal Medicine (Di.M.I.), University of Genova, Genova IT.
Anna GarutiDepartment of Internal Medicine (Di.M.I.), University of Genova, Genova IT.
Maurizio GalloDepartment of Internal Medicine (Di.M.I.), University of Genova, Genova IT.
Saverio AlbertiUnità di Patologia Oncologica CeSI, Università "G. D'Annunzio", Chieti Scalo (Chieti) IT.
Alessio NencioniDepartment of Internal Medicine (Di.M.I.), University of Genova, Genova IT.
Alberto BallestreroDepartment of Internal Medicine (Di.M.I.), University of Genova, Genova IT.
Gabriele ZoppoliDepartment of Internal Medicine (Di.M.I.), University of Genova, Genova IT.
University of Genoa · ITInstitut Jules Bordet · BEOspedale Policlinico San Martino · ITUniversity of Chieti-Pescara · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SQLE encodes squalene epoxidase, a key enzyme in cholesterol synthesis. SQLE has sporadically been reported among copy-number driven transcripts in multi-omics cancer projects. Yet, its functional relevance has never been subjected to systematic analyses. Here, we assessed the correlation of SQLE copy number (CN) and gene expression (GE) across multiple cancer types, focusing on the clinico-pathological associations in breast cancer (BC). We then investigated whether any biological effect of SQLE inhibition could be observed in BC cell line models. Breast, ovarian, and colorectal cancers showed the highest CN driven GE among 8,783 cases from 22 cancer types, with BC presenting the strongest one. SQLE overexpression was more prevalent in aggressive BC, and was an independent prognostic factor of unfavorable outcome. Through SQLE pharmacological inhibition and silencing in a panel of BC cell lines portraying the diversity of SQLE CN and GE, we demonstrated that SQLE inhibition resulted in a copy-dosage correlated decrease in cell viability, and in a noticeable increase in replication time, only in lines with detectable SQLE transcript. Altogether, our results pinpoint SQLE as a bona fide metabolic oncogene by amplification, and as a therapeutic target in BC. These findings could have implications in other cancer types.

Indexed as

OncogenesBiomarkers, TumorBreast NeoplasmsCell Line, TumorCell SurvivalCell Transformation, NeoplasticChromosomes, Human, Pair 8Disease ProgressionDNA Copy Number VariationsErb-b2 Receptor Tyrosine KinasesFemaleGene DosageGene ExpressionGene SilencingGenes, mycGenetic LociBiomarkers, TumorErb-b2 Receptor Tyrosine KinasesSqualene Monooxygenase

Identifiers

PMID26777065
PMCPMC4726025
OpenAlexW2340125363

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.