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Increase in AP-1 activity is a general event in thyroid cell transformation in vitro and in vivo.
- Source :
-
Oncogene [Oncogene] 1998 Jul 23; Vol. 17 (3), pp. 377-85. - Publication Year :
- 1998
-
Abstract
- We have recently reported that neoplastic transformation of two rat thyroid epithelial cell lines by retroviruses carrying the v-mos and v-ras Ki oncogenes is associated with a drastic increase of AP-1 activity. The most important effects were represented by the dramatic junB and fra-1 gene induction, which was abolished by the block of the transformation-induced HMGI-C protein synthesis. Here, we have further characterized the transformation-dependent AP-1 activity, by analysing the expression of different jun- and fos-related components, in rat thyroid cell lines transformed by several oncogenes, in human thyroid carcinoma cell lines, and in naturally occurring human thyroid tumours. A significant increase of Fra-1 and JunB protein levels was detected in all oncogene transformed rat thyroid cell lines. Fra-1 gene induction was demonstrated to occur also in human thyroid carcinoma cell lines and tissues. Conversely, c-Jun and JunD proteins, rather than JunB, accumulated in human thyroid carcinoma cell lines. An induction of AP-1 target genes was also detected both in rat and human thyroid transformed cell lines. Therefore, in vivo and in vitro thyroid cell transformation is associated with important compositional changes in the AP-1 complex and an increased transcriptional activity.
- Subjects :
- Animals
Epithelial Cells metabolism
Epithelial Cells pathology
Genes, jun
HMGA2 Protein
High Mobility Group Proteins biosynthesis
Humans
Neoplasm Proteins biosynthesis
Polymerase Chain Reaction
Proto-Oncogene Proteins c-fos biosynthesis
Proto-Oncogene Proteins c-jun biosynthesis
Rats
Thyroglobulin biosynthesis
Thyroid Gland pathology
Thyrotropin pharmacology
Cell Transformation, Neoplastic
Oncogenes
Thyroid Gland metabolism
Thyroid Neoplasms genetics
Transcription Factor AP-1 metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 0950-9232
- Volume :
- 17
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- Oncogene
- Publication Type :
- Academic Journal
- Accession number :
- 9690519
- Full Text :
- https://doi.org/10.1038/sj.onc.1201953