Evidence map›Paper›PMID 27384677›Full record

ArticleOncotarget2016

Stimulatory actions of IGF-I are mediated by IGF-IR cross-talk with GPER and DDR1 in mesothelioma and lung cancer cells.

Silvia Avino, Paola De Marco, Francesca Cirillo, Maria Francesca Santolla, Ernestina Marianna De Francesco, Maria Grazia Perri, Damiano Rigiracciolo, Vincenza Dolce, Antonino Belfiore, Marcello Maggiolini and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 43 citations in OpenAlex.

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  7. GPCRs and fibroblast heterogeneity in fibroblast-associated diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
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  17. GPER and Testicular Germ Cell Cancer.Frontiers in endocrinology · 2020
    Review
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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

12 authors at 2 institutions in 1 country.

Silvia AvinoDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Paola De MarcoDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Francesca CirilloDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Maria Francesca SantollaDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Ernestina Marianna De FrancescoDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Maria Grazia PerriDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Damiano RigiraccioloDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Vincenza DolceDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Antonino BelfioreEndocrinology, Department of Health Sciences, University Magna Graecia of Catanzaro, Catanzaro, Italy.
Marcello MaggioliniDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Rosamaria LappanoDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Adele VivacquaDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
University of Calabria · ITMagna Graecia University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin-like growth factor-I (IGF-I)/IGF-I receptor (IGF-IR) system has been largely involved in the pathogenesis and development of various tumors. We have previously demonstrated that IGF-IR cooperates with the G-protein estrogen receptor (GPER) and the collagen receptor discoidin domain 1 (DDR1) that are implicated in cancer progression. Here, we provide novel evidence regarding the molecular mechanisms through which IGF-I/IGF-IR signaling triggers a functional cross-talk with GPER and DDR1 in both mesothelioma and lung cancer cells. In particular, we show that IGF-I activates the transduction network mediated by IGF-IR leading to the up-regulation of GPER and its main target genes CTGF and EGR1 as well as the induction of DDR1 target genes like MATN-2, FBN-1, NOTCH 1 and HES-1. Of note, certain DDR1-mediated effects upon IGF-I stimulation required both IGF-IR and GPER as determined knocking-down the expression of these receptors. The aforementioned findings were nicely recapitulated in important biological outcomes like IGF-I promoted chemotaxis and migration of both mesothelioma and lung cancer cells. Overall, our data suggest that IGF-I/IGF-IR system triggers stimulatory actions through both GPER and DDR1 in aggressive tumors as mesothelioma and lung tumors. Hence, this novel signaling pathway may represent a further target in setting innovative anticancer strategies.

Indexed as

A549 CellsCell Line, TumorDiscoidin Domain Receptor 1Gene Expression Regulation, NeoplasticHumansInsulin-Like Growth Factor ILung NeoplasmsMesotheliomaReceptor Cross-TalkReceptor, IGF Type 1Receptors, EstrogenReceptors, G-Protein-CoupledRNA InterferenceSignal TransductionTime-Lapse ImagingDiscoidin Domain Receptor 1GPER1 protein, humanInsulin-Like Growth Factor IReceptor, IGF Type 1Receptors, EstrogenReceptors, G-Protein-CoupledDDR1GPERIGF-IIGF-IRlung cancermesotheliomaPathology Section

Identifiers

PMID27384677
PMCPMC5288143
OpenAlexW2464537074

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.