Evidence map›Paper›PMID 25193492›Full record

ArticleInvestigational new drugs2014

Targeting polo-like kinase 1 by NMS-P937 in osteosarcoma cell lines inhibits tumor cell growth and partially overcomes drug resistance.

Valeria Sero, Elisa Tavanti, Serena Vella, Claudia Maria Hattinger, Marilù Fanelli, Francesca Michelacci, Rogier Versteeg, Barbara Valsasina, Beth Gudeman, Piero Picci and 1 more

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Article in Investigational new drugs, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Yeast centrosomes act as organizing centers to promote Polo kinase-mediated adaptation to persistent DNA damage.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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

11 authors at 4 institutions in 3 countries.

Valeria SeroLaboratory of Experimental Oncology, Rizzoli Orthopaedic Institute, Via di Barbiano 1/10, 40136, Bologna, Italy.
Elisa Tavanti
Serena Vella
Claudia Maria Hattinger
Marilù Fanelli
Francesca Michelacci
Rogier Versteeg
Barbara Valsasina
Beth Gudeman
Piero Picci
Massimo Serra
Istituto Ortopedico Rizzoli · ITOrthopedic Institute · USAcademic Medical Center · NLNerviano Medical Sciences · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPolo-like kinase 1 (PLK1) has emerged as a prognostic factor in various neoplasms, but only scarce data have been reported for high-grade osteosarcoma (OS). In this study, we assessed PLK1 expression and the efficacy of PLK1 inhibitor NMS-P937 in OS.

methodsPLK1 expression was assessed on 21 OS clinical samples and on a panel of human OS cell lines. In vitro efficacy of NMS-P937 was evaluated on nine drug-sensitive and six drug-resistant human OS cell lines, either as single agent or in combination with the drugs used in chemotherapy for OS.

resultsPLK1 expression was higher in OS clinical samples and cell lines compared to normal human tissue. A higher PLK1 expression at diagnosis appeared to be associated with an unfavourable clinical outcome. PLK1 silencing produced growth inhibition, cell cycle retardation and apoptosis induction in human OS cell lines. NMS-P937 proved to be highly active in both drug-sensitive and drug-resistant cell lines, with the only exception of ABCB1-overexpressing, Doxorubicin (DX)-resistant variants. However, in these cells, the association of NMS-P937 with DX was able to revert DX-resistance by negatively interfering with ABCB1 transport activity. NMS-P937 was also able to decrease clonogenic and migration ability of human OS cell lines.

conclusionPLK1 can be proposed as a new candidate target for OS. Targeting PLK1 in OS with NMS-P937 in association with conventional chemotherapeutic drugs may be a new interesting therapeutic option, since this approach has proved to be active against drug resistant cells.

Indexed as

Antineoplastic AgentsApoptosisATP Binding Cassette Transporter, Subfamily BBone NeoplasmsCell CycleCell Cycle ProteinsCell Line, TumorCell ProliferationDoxorubicinDrug InteractionsDrug Resistance, NeoplasmGene Expression ProfilingHumansOsteosarcomaPolo-Like Kinase 1Protein Kinase InhibitorsABCB1 protein, humanAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily BCell Cycle ProteinsDoxorubicinNMS P937Polo-Like Kinase 1Protein Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene ProteinsPyrazolesQuinazolinesRNA, MessengerRNA, Small Interfering

Identifiers

PMID25193492
OpenAlexW2094965521

What OpenQuestion holds

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Registered trials

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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.