http://www.cnr.it/ontology/cnr/individuo/prodotto/ID21131
Identification of Polo-like kinase 1 as a potential therapeutic target in anaplastic thyroid carcinoma. (Articolo in rivista)
- Type
- Label
- Identification of Polo-like kinase 1 as a potential therapeutic target in anaplastic thyroid carcinoma. (Articolo in rivista) (literal)
- Anno
- 2009-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1158/0008-5472.CAN-08-1693 (literal)
- Alternative label
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Nappi TC; Salerno P; Zitzelsberger H; Carlomagno F; Salvatore G; Santoro M. (literal)
- Pagina inizio
- Pagina fine
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
- Note
- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Dipartimento di Biologia e Patologia Cellulare e Molecolare ''L. Califano'' c/o Istituto di Endocrinologia ed Oncologia Sperimentale del
CNR, Universita' ''Federico II''; Dipartimento di Studi delle Istituzioni e dei Sistemi Territoriali, Universita' ''Parthenope,'' Naples, Italy
and Institute of Molecular Radiobiology, GSF-Forschungszentrum fu¨r Umwelt und Gesundheit GmbH, Neuherberg, Germany (literal)
- Titolo
- Identification of Polo-like kinase 1 as a potential therapeutic target in anaplastic thyroid carcinoma. (literal)
- Abstract
- Anaplastic thyroid carcinoma (ATC) is one of the most
aggressive and chemoresistant cancers. The serine/threonine
kinase Polo-like kinase 1 (PLK1),a key regulator of multiple
steps during mitotic progression,is highly expressed in ATC.
Here,we used the BI 2536 PLK1 inhibitor on ATC and
nontransformed thyroid follicular cell lines. Our data show
that ATC cells are addicted to high levels of PLK1 activity for
proliferation,sur vival,anchorage-independent growth,and
tumorigenicity. On treatment with nanomolar doses of BI
2536,ATC cells progressed normally through S phase but died
thereafter,directly from mitotic arrest. Immunofluorescence
microscopy,immunoblot,and flow cytometry analysis showed
that,on PLK1 blockade, ATC cells arrested in prometaphase
with a 4N DNA content. Treated ATC cells accumulated
phosphohistone H3 and displayed characteristic mitotic (Polo)
spindle aberrations. Nontransformed thyroid cells were 3.2- to
18.4-fold less susceptible to BI 2536-induced cell cycle effects
compared with ATC cells. These findings identify PLK1 as a
promising target for the molecular therapy of ATC. (literal)
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