Scholz G, Martinerie C, Perbal B, Hanafusa H
Laboratory of Molecular Oncology, Rockefeller University, New York, New York 10021, USA.
Mol Cell Biol. 1996 Feb;16(2):481-6. doi: 10.1128/MCB.16.2.481.
We have sought to identify genes whose expression is altered as a consequence of transformation by p60v-src. Using the mRNA differential display method, we have identified the nov proto-oncogene as one gene that is down regulated in chicken embryo fibroblasts (CEFs) transformed by p60v-src. nov transcripts were also found to be present at only very low levels in proliferating CEFs in comparison with quiescent CEFs. Serum stimulation of quiescent CEFs also resulted in a decline in the steady-state level of nov transcripts. Taken together, these findings suggest that the nov gene is expressed only in quiescent fibroblasts and that its down regulation may contribute to cellular transformation by the v-src oncogene. Down regulation of the nov gene appears to occur at both the transcriptional and posttranscriptional levels. Results obtained from experiments with a protein kinase inhibitor suggest that protein kinase C may be a key downstream effector in mediating the down regulation of nov transcripts in response to activation of p60src or serum stimulation. In addition, we found that transcription of an unknown gene is required for the decline in the steady-state level of nov transcripts in response to serum stimulation.
我们试图鉴定那些因p60v-src转化而导致表达发生改变的基因。利用mRNA差异显示方法，我们已鉴定出nov原癌基因是一个在被p60v-src转化的鸡胚成纤维细胞（CEF）中表达下调的基因。与静止的CEF相比，在增殖的CEF中也发现nov转录本仅以非常低的水平存在。血清刺激静止的CEF也导致nov转录本的稳态水平下降。综合这些发现表明，nov基因仅在静止的成纤维细胞中表达，其下调可能有助于v-src癌基因介导的细胞转化。nov基因的下调似乎发生在转录和转录后水平。用蛋白激酶抑制剂进行的实验结果表明，蛋白激酶C可能是介导nov转录本响应p60src激活或血清刺激而下调的关键下游效应物。此外，我们发现，血清刺激后nov转录本稳态水平下降需要一个未知基因的转录。
