Manzoli L, Billi A M, Rubbini S, Bavelloni A, Faenza I, Gilmour R S, Rhee S G, Cocco L
Institute of Human Anatomy, University of Bologna, Italy.
Cancer Res. 1997 Jun 1;57(11):2137-9.
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) beta1 activity. In addition, several other reports have shown the involvement of PLC beta1 in nuclear signaling in different cell types. Although the demonstration of phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate hydrolysis by nuclear PLC beta1 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 beta1 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.
细胞核已被证明是肌醇脂质循环的一个位点，静止细胞用胰岛素样生长因子I（IGF-I）等生长因子处理时，该循环会受到影响。实际上，将瑞士3T3细胞暴露于IGF-I会导致细胞核磷脂酶C（PLC）β1活性迅速短暂增加。此外，其他几份报告表明PLCβ1参与了不同细胞类型的核信号传导。尽管细胞核PLCβ1对磷脂酰肌醇4-磷酸和磷脂酰肌醇4,5-二磷酸的水解作用证明了细胞核PLC信号传导的存在，但这一细胞核自主信号通路的意义尚未完全阐明。通过反义RNA诱导PLCβ1表达的抑制及其过表达，我们表明这种细胞核PLC对于IGF-I刺激静止的瑞士3T3细胞后DNA合成的起始至关重要。
