Evidence map›Paper›PMID 40004199›Full record

ArticleInternational journal of molecular sciences2025

Vittoria Cenni, Alberto Bavelloni, Cristina Capanni, Elisabetta Mattioli, Federico Bortolozzo, Snezana Kojic, Giulia Orlandi, Jessika Bertacchini, William L Blalock

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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.

Vittoria CenniInstitute of Molecular Genetics "Luigi Luca Cavalli-Sforza", National Research Council (IGM-CNR), Unit of Bologna, 40136 Bologna, Italy.ORCID 0000-0001-8062-1840
Alberto BavelloniLaboratory of Experimental Oncology, IRCCS Istituto Ortopedico Rizzoli, 40136 Bologna, Italy.ORCID 0000-0002-6467-1431
Cristina CapanniInstitute of Molecular Genetics "Luigi Luca Cavalli-Sforza", National Research Council (IGM-CNR), Unit of Bologna, 40136 Bologna, Italy.
Elisabetta MattioliInstitute of Molecular Genetics "Luigi Luca Cavalli-Sforza", National Research Council (IGM-CNR), Unit of Bologna, 40136 Bologna, Italy.ORCID 0000-0002-1395-1927
Federico BortolozzoInstitute of Molecular Genetics "Luigi Luca Cavalli-Sforza", National Research Council (IGM-CNR), Unit of Bologna, 40136 Bologna, Italy.
Snezana KojicGroup for Muscle Cellular and Molecular Biology, Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, 11042 Belgrade, Serbia.ORCID 0000-0001-5090-1278
Giulia OrlandiDepartment of Surgery, Medicine, Dentistry and Morphological Sciences with Interest in Transplant, Oncology and Regenerative Medicine, University of Modena and Reggio Emilia, 41124 Modena, Italy.ORCID 0000-0001-9252-4028
Jessika BertacchiniInstitute of Molecular Genetics "Luigi Luca Cavalli-Sforza", National Research Council (IGM-CNR), Unit of Bologna, 40136 Bologna, Italy.
William L BlalockInstitute of Molecular Genetics "Luigi Luca Cavalli-Sforza", National Research Council (IGM-CNR), Unit of Bologna, 40136 Bologna, Italy.ORCID 0000-0002-8045-4840

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ankrd2, a mechanoresponsive protein primarily studied in muscle physiology, is emerging as a player in cancer progression. This study investigates the functional role of Ankrd2 in osteosarcoma cells, revealing its critical involvement in cell proliferation and response to chemotherapeutic drugs. We showed that Ankrd2 knockdown impairs the activation of PI3K/Akt and ERK1/2 pathways, reduces levels of cell cycle regulators including cyclin D1 and cyclin B, and counteracts the expression of nuclear lamin A and lamin B, disrupting nuclear morphology and DNA integrity. Strikingly, the loss of Ankrd2 enhances the sensitivity of osteosarcoma cells to doxorubicin and cisplatin, highlighting Ankrd2 potential as a therapeutic target to improve chemotherapeutic efficacy. Defining a novel mechanistic role for Ankrd2 in promoting tumor progression, we propose that Ankrd2 reduction could be exploited as an adjuvant strategy to enhance the efficacy of chemotherapy, offering new therapeutic opportunities for OS treatment.

Indexed as

Bone NeoplasmsMuscle ProteinsNuclear ProteinsOsteosarcomaAntineoplastic AgentsCell Line, TumorCell ProliferationCisplatinDoxorubicinGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMAP Kinase Signaling SystemPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAntineoplastic AgentsCisplatinDoxorubicinMuscle ProteinsNuclear ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAnkrd2cancer progressionchemotherapy sensitivitynuclear laminaosteosarcomatargeted therapy

Identifiers

PMID40004199
PMCPMC11855734

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.