Mechanism of induction of transforming growth factor-beta type II receptorgene expression by v-Src in murine myeloid cells

Citation
Sh. Park et al., Mechanism of induction of transforming growth factor-beta type II receptorgene expression by v-Src in murine myeloid cells, CELL GROWTH, 12(1), 2001, pp. 9-18
Citations number
48
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cell & Developmental Biology
Journal title
CELL GROWTH & DIFFERENTIATION
ISSN journal
1044-9523 → ACNP
Volume
12
Issue
1
Year of publication
2001
Pages
9 - 18
Database
ISI
SICI code
1044-9523(200101)12:1<9:MOIOTG>2.0.ZU;2-J
Abstract
Transforming growth factor (TGF)-beta1 plays an important role during hemat opoiesis. Previously, we had shown that the growth of a v-Src-transformed m yeloid cell line was markedly more inhibited by TGF-beta treatment when com pared with the wild-type myeloid cell line. To investigate the increased gr owth sensitivity of the v-Src-transformed myeloid cell line, 32D-src, to TG F-beta, we examined expression of the TGF-beta type II receptor (TGF-beta R II) gene in myeloid cell lines. Northern blot analysis showed that expressi on of similar to8- and 6-kb species of TGF-beta RII transcripts was markedl y increased in the 32D-src cell line. The expression of the TGF-beta RII pr omoter linked to a reporter gene was increased 23-fold by v-Src, DNA transf ection and electrophoretic mobility shift assay revealed that v-Src induces TGF-beta RII promoter activity through an AP1/ATF2-like sequence (-219 to -172), ETS binding sites (+1 to +36), and the inverted CCAAT box (-81 to -7 7), Novel DNA-protein complexes with FTS binding sites are significantly in creased in v-src-transformed cell lines compared with the control cell line . These results suggest that v-Src induces activity of the TGF-beta RII pro moter through multiple elements by inducing expression of nuclear proteins interacting with these elements.