Santi P, Zini N, Santi S, Riccio M, Guiliani Piccari G, De Pol A, Maraldi N M
Department of Scienze Anatomiche Umane e Fisiopatologia dell'Apparato Locomotore, University of Bologna, 40126 Bologna, Italy.
Int J Oncol. 2001 Jan;18(1):165-74. doi: 10.3892/ijo.18.1.165.
To elucidate the relationship between inositol lipid signal transduction and oncogenic transformation, the activity and subcellular distribution of phospholipase C isoforms and of phosphatidylinositol 3-kinase were analysed in Morris hepatoma cells, MH(1)C(1), with respect to normal rat liver cells. The results provide evidence of a gain of function of the enzymes involved in inositide signal transduction, the amount of which increased mainly at the nuclear level. Phospholipase C and phosphatidylinositol 3-kinase activities are significantly higher in rat hepatoma than in rat liver cells. Moreover, some phospholipase C isoforms are expressed at higher levels at the nuclear level; this is particularly evident in the case of the delta 1 isoform which is not expressed at the nuclear level in rat liver cells. Therefore, the autonomous nuclear signal transduction system, formerly reported as involved in the modulation of cell proliferation and differentiation, appears also affected in oncogenic transformation.
为阐明肌醇脂质信号转导与致癌转化之间的关系，对莫里斯肝癌细胞MH(1)C(1)中磷脂酶C同工型和磷脂酰肌醇3激酶的活性及亚细胞分布进行了分析，并与正常大鼠肝细胞进行了比较。结果提供了参与肌醇信号转导的酶功能获得的证据，其数量主要在核水平增加。大鼠肝癌细胞中磷脂酶C和磷脂酰肌醇3激酶的活性明显高于大鼠肝细胞。此外，一些磷脂酶C同工型在核水平表达较高；在δ1同工型的情况下尤为明显，该同工型在大鼠肝细胞的核水平不表达。因此，先前报道参与细胞增殖和分化调节的自主核信号转导系统在致癌转化中似乎也受到影响。
