Evidence map›Paper›PMID 25797262›Full record

ArticleOncotarget2015

Pleiotropic modes of action in tumor cells of RNASET2, an evolutionary highly conserved extracellular RNase.

Marta Lualdi, Edoardo Pedrini, Katia Rea, Laura Monti, Debora Scaldaferri, Marzia Gariboldi, Annalisa Camporeale, Paolo Ghia, Elena Monti, Antonella Tomassetti and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  15. Innate Immune Response Regulation by the HumanFrontiers in immunology · 2019
    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 4 institutions in 1 country.

Marta LualdiDepartment of Theoretical and Applied Sciences, Università degli Studi dell'Insubria, Varese, Italy.
Edoardo PedriniDepartment of Theoretical and Applied Sciences, Università degli Studi dell'Insubria, Varese, Italy.
Katia ReaUnit of Molecular Therapies, Department of Experimental Oncology and Molecular Medicine, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy.
Laura MontiDepartment of Theoretical and Applied Sciences, Università degli Studi dell'Insubria, Varese, Italy.
Debora ScaldaferriDepartment of Theoretical and Applied Sciences, Università degli Studi dell'Insubria, Varese, Italy.
Marzia GariboldiDepartment of Theoretical and Applied Sciences, Università degli Studi dell'Insubria, Busto Arsizio, Italy.
Annalisa CamporealeDivision of Molecular Oncology and Department of Onco-Hematology, IRCCS Ospedale San Raffaele, Milan, Italy.
Paolo GhiaDivision of Molecular Oncology and Department of Onco-Hematology, IRCCS Ospedale San Raffaele, Milan, Italy.
Elena MontiDepartment of Theoretical and Applied Sciences, Università degli Studi dell'Insubria, Busto Arsizio, Italy.
Antonella TomassettiUnit of Molecular Therapies, Department of Experimental Oncology and Molecular Medicine, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy.
Francesco AcquatiDepartment of Theoretical and Applied Sciences, Università degli Studi dell'Insubria, Varese, Italy.
Roberto TaramelliDepartment of Theoretical and Applied Sciences, Università degli Studi dell'Insubria, Varese, Italy.
University of Insubria · ITFondazione IRCCS Istituto Nazionale dei Tumori · ITIRCCS Ospedale San Raffaele · ITVita-Salute San Raffaele University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As widely recognized, tumor growth entails a close and complex cross-talk among cancer cells and the surrounding tumor microenvironment. We recently described the human RNASET2 gene as one key player of such microenvironmental cross-talk. Indeed, the protein encoded by this gene is an extracellular RNase which is able to control cancer growth in a non-cell autonomous mode by inducing a sustained recruitment of immune-competent cells belonging to the monocyte/macrophage lineage within a growing tumor mass. Here, we asked whether this oncosuppressor gene is sensitive to stress challenges and whether it can trigger cell-intrinsic processes as well. Indeed, RNASET2 expression levels were consistently found to increase following stress induction. Moreover, changes in RNASET2 expression levels turned out to affect several cancer-related parameters in vitro in an ovarian cancer cell line model. Of note, a remarkable rearrangement of the actin cytoskeleton organization, together with changes in cell adhesion and motility, emerged as putative mechanisms by which such cell-autonomous role could occur. Altogether, these biological features allow to put forward the hypothesis that the RNASET2 protein can act as a molecular barrier for limiting the damages and tissue remodeling events occurring during the earlier step of cell transformation.

Indexed as

AnimalsCell Growth ProcessesCell HypoxiaCell Line, TumorCell MovementFemaleHeLa CellsHeterograftsHumansMaleMiceMice, NudeOvarian NeoplasmsRibonucleasesSignal TransductionTumor MicroenvironmentRibonucleasesRNASET2 protein, humanTumor Suppressor Proteinsmicroenvironmentovarian cancerRNasestress response

Identifiers

PMID25797262
PMCPMC4480721
OpenAlexW1520790052

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.