Evidence map›Paper›PMID 33419058›Full record

ArticleCancers2021

Ectopic Expression of Ankrd2 Affects Proliferation, Motility and Clonogenic Potential of Human Osteosarcoma Cells.

Manuela Piazzi, Snezana Kojic, Cristina Capanni, Nemanja Stamenkovic, Alberto Bavelloni, Oriano Marin, Giovanna Lattanzi, William Blalock, Vittoria Cenni

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Downregulation ofTranslational cancer research · 2025
    Article
  2. International journal of molecular sciences · 2025
    Article
  3. Article
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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

9 authors at 3 institutions in 2 countries.

Manuela PiazziUnit of Bologna, Institute of Molecular Genetics "Luigi Luca Cavalli-Sforza", National Research Council of Italy (IGM-CNR), 40136 Bologna, Italy.ORCID 0000-0002-9072-2757
Snezana KojicInstitute of Molecular Genetics and Genetic Engineering, University of Belgrade, 11042 Belgrade, Serbia.ORCID 0000-0001-5090-1278
Cristina CapanniUnit of Bologna, Institute of Molecular Genetics "Luigi Luca Cavalli-Sforza", National Research Council of Italy (IGM-CNR), 40136 Bologna, Italy.
Nemanja StamenkovicInstitute of Molecular Genetics and Genetic Engineering, University of Belgrade, 11042 Belgrade, Serbia.
Alberto BavelloniLaboratory of Experimental Oncology, IRCCS Istituto Ortopedico Rizzoli, 40136 Bologna, Italy.ORCID 0000-0002-6467-1431
Oriano MarinDepartment of Biomedical Sciences, University of Padua, 35131 Padua, Italy.
Giovanna LattanziUnit of Bologna, Institute of Molecular Genetics "Luigi Luca Cavalli-Sforza", National Research Council of Italy (IGM-CNR), 40136 Bologna, Italy.ORCID 0000-0002-7103-8722
William BlalockUnit of Bologna, Institute of Molecular Genetics "Luigi Luca Cavalli-Sforza", National Research Council of Italy (IGM-CNR), 40136 Bologna, Italy.ORCID 0000-0002-8045-4840
Vittoria CenniUnit of Bologna, Institute of Molecular Genetics "Luigi Luca Cavalli-Sforza", National Research Council of Italy (IGM-CNR), 40136 Bologna, Italy.ORCID 0000-0001-8062-1840
Istituto Ortopedico Rizzoli · ITUniversity of Belgrade · RSUniversity of Padua · IT

Funding

Associazione Italiana per la Ricerca sul Cancro AIRC IG-2015; Grant #17137Ministry of Education, Science and Technological Development of the Republic of Serbia projects 173008 and 451-03-68/2020-14/200042
6 · The paper itself

Abstract

Ankrd2 is a protein known for being mainly expressed in muscle fibers, where it participates in the mechanical stress response. Since both myocytes and osteoblasts are mesenchymal-derived cells, we were interested in examining the role of Ankrd2 in the progression of osteosarcoma which features a mechano-stress component. Although having been identified in many tumor-derived cell lines and -tissues, no study has yet described nor hypothesized any involvement for this protein in osteosarcoma tumorigenesis. In this paper, we report that Ankrd2 is expressed in cell lines obtained from human osteosarcoma and demonstrate a contribution by this protein in the pathogenesis of this insidious disease. Ankrd2 involvement in osteosarcoma development was evaluated in clones of Saos2, U2OS, HOS and MG63 cells stably expressing Ankrd2, through the investigation of hallmark processes of cancer cells. Interestingly, we found that exogenous expression of Ankrd2 influenced cellular growth, migration and clonogenicity in a cell line-dependent manner, whereas it was able to improve the formation of 3D spheroids in three out of four cellular models and enhanced matrix metalloproteinase (MMP) activity in all tested cell lines. Conversely, downregulation of Ankrd2 expression remarkably reduced proliferation and clonogenic potential of parental cells. As a whole, our data present Ankrd2 as a novel player in osteosarcoma development, opening up new therapeutic perspectives.

Indexed as

Ankrd2bonecancermechanotransductionmigrationosteosarcomaproliferationspheroids

Identifiers

PMID33419058
PMCPMC7825408
OpenAlexW3120298466

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.