http://www.cnr.it/ontology/cnr/individuo/prodotto/ID20875
Ras-mediated apoptosis of PC CL 3 rat thyroid cells induced by RET/PTC oncogenes (Articolo in rivista)
- Type
- Label
- Ras-mediated apoptosis of PC CL 3 rat thyroid cells induced by RET/PTC oncogenes (Articolo in rivista) (literal)
- Anno
- 2003-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1038/sj.onc.1206112 (literal)
- Alternative label
Castellone M.D. , Cirafici A.M. , De Vita G. , De Falco V. , Malorni L. , Tallini G. , Fagin J.A., Fusco A. , Melillo R.M. , Santoro M. (2003)
Ras-mediated apoptosis of PC CL 3 rat thyroid cells induced by RET/PTC oncogenes
in Oncogene (Basingstoke)
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Castellone M.D. , Cirafici A.M. , De Vita G. , De Falco V. , Malorni L. , Tallini G. , Fagin J.A., Fusco A. , Melillo R.M. , Santoro M. (literal)
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- ISI Web of Science (WOS) (literal)
- SCImago (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Castellone M.D:Istituto di Endocrinologia ed Oncologia Sperimentale del CNR, c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare, University 'Federico II', Naples, Italy
Cirafici A.M. Istituto di Endocrinologia ed Oncologia Sperimentale del CNR, c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare, University 'Federico II', Naples, Italy
De Vita G:Istituto di Endocrinologia ed Oncologia Sperimentale del CNR, c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare, University 'Federico II', Naples, Italy
De Falco V.:Istituto di Endocrinologia ed Oncologia Sperimentale del CNR, c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare, University 'Federico II', Naples, Italy
Malorni L.:Istituto di Endocrinologia ed Oncologia Sperimentale del CNR, c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare, University 'Federico II', Naples, Italy
Tallini G:Department of Pathology, University of Yale, USA
Fagin J.A.:Division of Endocrinology, University of Cincinnati College of Medicine, Ohio 45267-0547, USA
Fusco A.:Istituto di Endocrinologia ed Oncologia Sperimentale del CNR, c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare, University 'Federico II', Naples, Italy
Melillo R.M.:Istituto di Endocrinologia ed Oncologia Sperimentale del CNR, c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare, University 'Federico II', Naples, Italy
Santoro M.:Istituto di Endocrinologia ed Oncologia Sperimentale del CNR, c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare, University 'Federico II', Naples, Italy
:Department of Pathology, University of Yale, USA (literal)
- Titolo
- Ras-mediated apoptosis of PC CL 3 rat thyroid cells induced by RET/PTC oncogenes (literal)
- Abstract
- RET gene rearrangements, which generate chimeric RET/PTC oncogenes, are early events in the evolution of thyroid papillary carcinomas. Expression of RET/PTC oncogenes promotes neoplastic transformation of cultured thyroid cells and of thyroid glands in transgenic mice. Notwithstanding these oncogenic effects, we have found that the expression of two RET/PTC oncogenes (H4-RET and RFG-RET) induces apoptosis of rat thyroid PC CL 3 cells. Promotion of thyroid cell death depends on the kinase activity of RET/PTC and on the phosphorylation of a tyrosine residue (tyrosine 1062) that maps in the carboxy-terminus of the RET protein. Tyrosine 1062 is essential for RET/PTC-mediated activation of the Ras/ERK pathway. Inhibition of Ras/ERK by a dominant negative Ras or by the MEKI inhibitor, PD98059, obstructed RET/PTC-mediated apoptosis. We also show that signals transmitted by tyrosine 1062 mediate proapoptotic events like Bcl-2 down regulation and Bax upregulation, and that adoptive overexpression of Bcl-2 overcomes RET/PTC-induced apoptosis. Thus, gene rearrangements that generate RET/PTC oncogenes subvert RET function by converting it into a chronically active kinase that is constitutively phosphorylated on tyrosine 1062. In turn, Y1062 phosphorylation transmits not only mitogenic but also proapoptotic signals to thyroid cells. (literal)
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