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

Ankrd2 bone cancer mechanotransduction migration osteosarcoma proliferation spheroids

Journal

Cancers
ISSN: 2072-6694
Titre abrégé: Cancers (Basel)
Pays: Switzerland
ID NLM: 101526829

Informations de publication

Date de publication:
06 Jan 2021
Historique:
received: 01 12 2020
revised: 28 12 2020
accepted: 04 01 2021
entrez: 9 1 2021
pubmed: 10 1 2021
medline: 10 1 2021
Statut: epublish

Résumé

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.

Identifiants

pubmed: 33419058
pii: cancers13020174
doi: 10.3390/cancers13020174
pmc: PMC7825408
pii:
doi:

Types de publication

Journal Article

Langues

eng

Subventions

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

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Auteurs

Manuela Piazzi (M)

Unit of Bologna, Institute of Molecular Genetics "Luigi Luca Cavalli-Sforza", National Research Council of Italy (IGM-CNR), 40136 Bologna, Italy.
IRCCS, Istituto Ortopedico Rizzoli, 40136 Bologna, Italy.

Snezana Kojic (S)

Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, 11042 Belgrade, Serbia.

Cristina Capanni (C)

Unit of Bologna, Institute of Molecular Genetics "Luigi Luca Cavalli-Sforza", National Research Council of Italy (IGM-CNR), 40136 Bologna, Italy.
IRCCS, Istituto Ortopedico Rizzoli, 40136 Bologna, Italy.

Nemanja Stamenkovic (N)

Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, 11042 Belgrade, Serbia.

Alberto Bavelloni (A)

Laboratory of Experimental Oncology, IRCCS Istituto Ortopedico Rizzoli, 40136 Bologna, Italy.

Oriano Marin (O)

Department of Biomedical Sciences, University of Padua, 35131 Padua, Italy.

Giovanna Lattanzi (G)

Unit of Bologna, Institute of Molecular Genetics "Luigi Luca Cavalli-Sforza", National Research Council of Italy (IGM-CNR), 40136 Bologna, Italy.
IRCCS, Istituto Ortopedico Rizzoli, 40136 Bologna, Italy.

William Blalock (W)

Unit of Bologna, Institute of Molecular Genetics "Luigi Luca Cavalli-Sforza", National Research Council of Italy (IGM-CNR), 40136 Bologna, Italy.
IRCCS, Istituto Ortopedico Rizzoli, 40136 Bologna, Italy.

Vittoria Cenni (V)

Unit of Bologna, Institute of Molecular Genetics "Luigi Luca Cavalli-Sforza", National Research Council of Italy (IGM-CNR), 40136 Bologna, Italy.
IRCCS, Istituto Ortopedico Rizzoli, 40136 Bologna, Italy.

Classifications MeSH