Abstract:
:Cyclin D1 expression is jointly regulated by growth factors and cell adhesion to the extracellular matrix in many cell types. Growth factors are thought to regulate cyclin D1 expression because they stimulate sustained extracellular signal-regulated kinase (ERK) activity. However, we show here that growth factors induce transient ERK activity when added to suspended fibroblasts and sustained ERK activity only when added to adherent fibroblasts. Cell attachment to fibronectin or anti-alpha5beta1 integrin is sufficient to sustain the ERK signal and to induce cyclin D1 in growth factor-treated cells. Moreover, when we force the sustained activation of ERK, by conditional expression of a constitutively active MAP kinase/ERK kinase, we overcome the adhesion requirement for expression of cyclin D1. Thus, at least in part, fibroblasts are mitogen and anchorage dependent, because integrin action allows for a sustained ERK signal and the expression of cyclin D1 in growth factor-treated cells.
journal_name
Mol Biol Celljournal_title
Molecular biology of the cellauthors
Roovers K,Davey G,Zhu X,Bottazzi ME,Assoian RKdoi
10.1091/mbc.10.10.3197keywords:
subject
Has Abstractpub_date
1999-10-01 00:00:00pages
3197-204issue
10eissn
1059-1524issn
1939-4586journal_volume
10pub_type
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