## Abstract Insulinβlike growth factor binding proteinβ3 (IGFBPβ3), an antiproliferative and proapoptotic protein, has been shown to be upregulated by growth inhibitory concentrations of androgens in LNCaP human prostate cancer (PCa) cells, but the mechanism of regulation and the role of IGFBPβ3 in
Studies on the cell-cycle dependency of the actions of insulin-like growth factor-I in Balb/c 3T3 cells
β Scribed by Itaru Kojima; Masafumi Kitaoka; Etsuro Ogata
- Publisher
- John Wiley and Sons
- Year
- 1990
- Tongue
- English
- Weight
- 466 KB
- Volume
- 143
- Category
- Article
- ISSN
- 0021-9541
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β¦ Synopsis
I 12, lapan
The present study was conducted to determine the cell-cycle dependency of various actions of IGF-I in Balbk 3T3 cells. When autophosphorylation of the IGF-I receptor was determined in [ '2P]-labelled cells, IGF-I increased radioactivity in a 100 K-Da phosphoprotein, presumably p-subunit of the IGF-I receptor, both in quiesent and in primed competent cells. Likewise, IGF-I stimulated uptake of [3H]deoxyglucose independent of the cell cycle. In contrast, IGF-I increased calcium entry, radioactivity in [ 'H]diacylglycerol, and I3H]thymidine incorporation in primed competent cells while these reactions were not induced by IGF-I in quiescent cells. The latter three reactions were attenuated when cells were pretreated with pertussis toxin, These results indicate that some, but not all, of the actions of IGF-I are dependent on the cell cycle in Balb/c 3T3 cells. They also suggest that a pertussis-toxin-sensitive G protein may be involved in the cellcycle-dependent actions of IGF-I.
Insulin-like growth factor-I (IGF-I) is a potent mitogen which regulates mammalian somatic growth in vivo (1). TGF-I also stimulates cell proliferation in various types of cells in tissue culture. The mechanism by which IGF-I promotes cell growth is of great interest but still remains largely uncertain. The mode of action
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