Evidence map›Paper›PMID 35422060›Full record

ArticleCell death & disease2022

Lamin A and the LINC complex act as potential tumor suppressors in Ewing Sarcoma.

Francesca Chiarini, Francesca Paganelli, Tommaso Balestra, Cristina Capanni, Antonietta Fazio, Maria Cristina Manara, Lorena Landuzzi, Stefania Petrini, Camilla Evangelisti, Pier-Luigi Lollini and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  3. Article
  4. Article
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  6. Article
  7. Lamins' role in osteosarcoma.Frontiers in cell and developmental biology · 2026
    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

13 authors at 4 institutions in 1 country.

Francesca Chiarini *CNR Institute of Molecular Genetics "Luigi Luca Cavalli-Sforza", Unit of Bologna, 40136, Bologna, Italy. francesca.chiarini@cnr.it.ORCID 0000-0002-4568-3189
Francesca Paganelli *CNR Institute of Molecular Genetics "Luigi Luca Cavalli-Sforza", Unit of Bologna, 40136, Bologna, Italy.
Tommaso BalestraIRCCS Istituto Ortopedico Rizzoli, Experimental Oncology Laboratory, 40136, Bologna, Italy.
Cristina CapanniCNR Institute of Molecular Genetics "Luigi Luca Cavalli-Sforza", Unit of Bologna, 40136, Bologna, Italy.
Antonietta FazioAlma Mater Studiorum, University of Bologna, Department of Biomedical and Neuromotor Sciences, 40136, Bologna, Italy.
Maria Cristina ManaraIRCCS Istituto Ortopedico Rizzoli, Experimental Oncology Laboratory, 40136, Bologna, Italy.ORCID 0000-0001-5686-720X
Lorena LanduzziIRCCS Istituto Ortopedico Rizzoli, Experimental Oncology Laboratory, 40136, Bologna, Italy.
Stefania PetriniConfocal Microscopy Core Facility, Research Center, Bambino Gesu' Children's Hospital IRCCS, 00146, Rome, Italy.ORCID 0000-0002-3249-0003
Camilla EvangelistiAlma Mater Studiorum, University of Bologna, Department of Biomedical and Neuromotor Sciences, 40136, Bologna, Italy.
Pier-Luigi LolliniAlma Mater Studiorum, University of Bologna, Department of Experimental, Diagnostic and Specialty Medicine, 40138, Bologna, Italy.
Alberto M MartelliAlma Mater Studiorum, University of Bologna, Department of Biomedical and Neuromotor Sciences, 40136, Bologna, Italy.
Giovanna LattanziCNR Institute of Molecular Genetics "Luigi Luca Cavalli-Sforza", Unit of Bologna, 40136, Bologna, Italy. giovanna.lattanzi@cnr.it.ORCID 0000-0002-7103-8722
Katia ScotlandiIRCCS Istituto Ortopedico Rizzoli, Experimental Oncology Laboratory, 40136, Bologna, Italy. katia.scotlandi@ior.it.ORCID 0000-0001-6114-9499
Istituto Ortopedico Rizzoli · ITUniversity of Bologna · ITBambino Gesù Children's Hospital · ITIstituto di Genetica Molecolare · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lamin A, a main constituent of the nuclear lamina, is involved in mechanosignaling and cell migration through dynamic interactions with the LINC complex, formed by the nuclear envelope proteins SUN1, SUN2 and the nesprins. Here, we investigated lamin A role in Ewing Sarcoma (EWS), an aggressive bone tumor affecting children and young adults. In patients affected by EWS, we found a significant inverse correlation between LMNA gene expression and tumor aggressiveness. Accordingly, in experimental in vitro models, low lamin A expression correlated with enhanced cell migration and invasiveness and, in vivo, with an increased metastatic load. At the molecular level, this condition was linked to altered expression and anchorage of nuclear envelope proteins and increased nuclear retention of YAP/TAZ, a mechanosignaling effector. Conversely, overexpression of lamin A rescued LINC complex organization, thus reducing YAP/TAZ nuclear recruitment and preventing cell invasiveness. These effects were also obtained through modulation of lamin A maturation by a statin-based pharmacological treatment that further elicited a more differentiated phenotype in EWS cells. These results demonstrate that drugs inducing nuclear envelope remodeling could be exploited to improve therapeutic strategies for EWS.

Indexed as

Nuclear EnvelopeSarcoma, EwingHumansLamin Type AMembrane ProteinsMicrotubule-Associated ProteinsNuclear ProteinsLamin Type AMembrane ProteinsMicrotubule-Associated ProteinsNuclear Proteins

Identifiers

PMID35422060
PMCPMC9010457
OpenAlexW4223970590

What OpenQuestion holds

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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.