Fos family members: regulation,
structure and role in oncogenic transformation

Tulchinsky, E.

Publication:
Fos family members: regulation, structure and role in oncogenic transformation

dc.contributor.author	Tulchinsky, E.
dc.date.accessioned	2020-07-23T13:24:19Z
dc.date.available	2020-07-23T13:24:19Z
dc.date.issued	2000
dc.description.abstract	The members of the Fos protein family might be subdivided in two groups, according to their ability to transform rodent fibroblasts, transforming (c-Fos and FosB) and non-transforming (Fra-I and Fra-2) proteins. Members of these groups are differently activated in response to external stimuli and posses different structural features. Importantly, whilst c-Fos and FosB contain multiple transactivation modules in their N- and C-terminal parts, transactivation domains are absent in the non-transforming Fos proteins. As a result, Fra-l and Fra-2 though efficiently form dimers with the Jun proteins, are weak transcriptional activators and inhibit the c-Fos-dependent activation in transient transfection assay. The numerous experiments performed with the different Fos mutant proteins with impaired transforming ability, as well as with chimeric proteins revealed the importance of the transactivation function for transformation. Fra-l and Fra-2 proteins albeit ineffectively triggering oncogenic transformation, are abundant in ras- and src-transformed murine and chicken fibroblasts, in neoplastic thyroid cells and in highly malignant mouse adenocarcinoma cells, which underwent mesenchymal transition. The abundance of the non-transforming Fos proteins in these systems might be mediated by a positive AP-l-dependent feedback mechanism, as well as by Mlt signals. Furthermore, the manipulation of the Fra-l expression level in thyroid and mammary tumor cells modulated the transcription of several tumor progression markers and affected cell morphology and invasiveness. These recent data demonstrate a novel function of non-transforming Fos proteins in the maintenance and progression of the transformed state. Interestingly, this function is independent of the documented invalidity of the Fra-l and Fra-2 proteins as transcriptional activators in rodent fibroblasts.	es
dc.format	application/pdf	es
dc.format.extent	8	es
dc.identifier.citation	Histology and Histopathology, Vol. 15, n.º 3 (2000)
dc.identifier.issn	1699-5848
dc.identifier.issn	0213-3911
dc.identifier.uri	http://hdl.handle.net/10201/95173
dc.language	eng	es
dc.publisher	F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología	es
dc.rights	info:eu-repo/semantics/openAccess	es
dc.rights	Attribution-NonCommercial-NoDerivatives 4.0 International	*
dc.rights.uri	http://creativecommons.org/licenses/by-nc-nd/4.0/	*
dc.subject	AP-1	es
dc.subject	Fos	es
dc.subject	Fra-1	es
dc.subject	Fra-2	es
dc.subject	Neoplastic transformation	es
dc.subject.other	CDU::5 - Ciencias puras y naturales::57 - Biología::576 - Biología celular y subcelular. Citología	es
dc.title	Fos family members: regulation, structure and role in oncogenic transformation	es
dc.type	info:eu-repo/semantics/article	es
dspace.entity.type	Publication	es

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