Essential role for nuclear phospholipase C β1 in insulin-like growth factor I-induced mitogenesis

Lucia Manzoli, Anna Maria Billi, Silvia Rubbini, Alberto Bavelloni, Irene Faenza, R. Stewart Gilmour, Sue Goo Rhee, Lucio Cocco

Research output: Contribution to journalArticle

Abstract

The nucleus has been shown to be a site for the inositol lipid cycle that can be affected by treatment of quiescent cells with growth factors such as insulin-like growth factor I (IGF-I). Indeed, the exposure of Swiss 3T3 cells to IGF-I results in a rapid and transient increase in nuclear phospholipase C (PLC) β1 activity. In addition, several other reports have shown the involvement of PLC β1 in nuclear signaling in different cell types. Although the demonstration of phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate hydrolysis by nuclear PLC β1 established the existence of nuclear PLC signaling, the significance of this autonomous pathway in the nucleus has yet to be thoroughly clarified. By inducing both the inhibition of PLC β1 expression by antisense RNA and its overexpression, we show that this nuclear PLC is essential for the onset of DNA synthesis following IGF-I stimulation of quiescent Swiss 3T3 cells.

Original languageEnglish
Pages (from-to)2137-2139
Number of pages3
JournalCancer Research
Volume57
Issue number11
Publication statusPublished - Jun 1 1997

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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    Manzoli, L., Billi, A. M., Rubbini, S., Bavelloni, A., Faenza, I., Gilmour, R. S., Rhee, S. G., & Cocco, L. (1997). Essential role for nuclear phospholipase C β1 in insulin-like growth factor I-induced mitogenesis. Cancer Research, 57(11), 2137-2139.