Lu Y, Chaney W
Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha 68198-4525.
Mol Cell Biochem. 1993 May 12;122(1):85-92. doi: 10.1007/BF00925741.
Viral infection of cultured cells with transforming viruses causes an increase in cell-surface N-linked beta 1-6 (GlcNAc beta 1-6Man) branching of complex-type oligosaccharides. Similar observations have been made after transfection of cells with activated oncogenes, which is associated with an induction of tumorigenic and metastatic properties. In this study, the effects of transfection of both activated and proto-Ha-ras oncogenes into NIH3T3 cells were analyzed. The results showed that, in comparison with NIH3T3 cells, both ras transfectants have increased sensitivity to the cytotoxic action of L-PHA. An increase in beta 1-6 branching and an increased level of N-acetylglucosaminyltransferase V (GlcNAc-T V), the enzyme which initiates the beta 1-6 branching were also observed. The levels of GlcNAc-T I and beta 1-4 Gal-T remained unchanged in activated Ha-ras transfected NIH3T3 cells. These data suggest that a specific induction of GlcNAc-T V occurs after transfection with either the proto- or activated Ha-ras oncogenes, which is responsible for the increased beta 1-6 branching previously observed.
用转化病毒对培养细胞进行病毒感染会导致复杂型寡糖的细胞表面N-连接β1-6(GlcNAcβ1-6Man)分支增加。在用活化癌基因转染细胞后也有类似的观察结果,这与致瘤性和转移性特性的诱导有关。在本研究中,分析了将活化的和原癌基因Ha-ras转染到NIH3T3细胞中的效果。结果表明,与NIH3T3细胞相比,两种ras转染细胞对L-PHA的细胞毒性作用的敏感性均增加。还观察到β1-6分支增加以及N-乙酰葡糖胺转移酶V(GlcNAc-T V)水平升高,该酶启动β1-6分支。在活化的Ha-ras转染的NIH3T3细胞中,GlcNAc-T I和β1-4 Gal-T的水平保持不变。这些数据表明,在用原癌基因或活化的Ha-ras癌基因转染后会发生GlcNAc-T V的特异性诱导,这是先前观察到的β1-6分支增加的原因。