Uchida T, Matozaki T, Suzuki T, Matsuda K, Wada K, Nakano O, Konda Y, Nishisaki H, Nagao M, Sakamoto C
Second Department of Internal Medicine, Kobe University School of Medicine, Japan.
Biochem Biophys Res Commun. 1992 Aug 31;187(1):332-9. doi: 10.1016/s0006-291x(05)81497-4.
To understand the molecular mechanism of gastric tumorigenesis, the status of neurofibromatosis type 1 (NF1) gene was analyzed in human gastric cancer cell lines. Although the sequencing of the GTPase activating protein (GAP)-related region of NF1 (NF1-GRD) revealed no apparent mutation, the NF1-GRD transcript (type I) and that containing an additional 63 bp insert in the center of NF1-GRD (type II) were equally expressed in most gastric cancer cells. By contrast, type II was predominantly expressed in normal stomach mucosa. When these two types of NF1-GRD were bacterially expressed and their GAP activities were tested, both types of NF1-GRD similarly stimulated ras GTPase activity. However, arachidonic acid inhibited GAP activities of two types of NF1-GRD to different extents. These results suggest that the increased expression of type I NF1 protein may modulate ras-related signal transduction and it may be related to the control of the gastric cellular proliferation.
为了解胃癌发生的分子机制,对人胃癌细胞系中1型神经纤维瘤病(NF1)基因的状态进行了分析。虽然NF1的GTP酶激活蛋白(GAP)相关区域(NF1-GRD)的测序未发现明显突变,但NF1-GRD转录本(I型)和在NF1-GRD中心含有额外63 bp插入片段的转录本(II型)在大多数胃癌细胞中表达水平相当。相比之下,II型在正常胃黏膜中占主导表达。当这两种类型的NF1-GRD在细菌中表达并检测其GAP活性时,两种类型的NF1-GRD同样刺激ras GTP酶活性。然而,花生四烯酸对两种类型的NF1-GRD的GAP活性有不同程度的抑制作用。这些结果表明,I型NF1蛋白表达增加可能调节ras相关信号转导,并且可能与胃细胞增殖的控制有关。