神経芽細胞腫における癌遺伝子とMHC抗原遺伝子間の発現調節機構に関する検討 : マウス神経芽細胞腫を用いたH-2 Gene, N-myc, c-src相互間制御の分子生物学的解析

概要

論文の詳細を見る
The authors have investigated the relationship between oncogene (N-myc and c-src) expression and major histocompatibility complex (H-2 in the mouse) antigen gene expression at the molecular levels, by using mouse neuroblastoma sublines (NB-1 and NB-V). Fluorescence-activated cell sorter analysis showed that NB-1 cells exhibited positive expression to H-2 K^k, H-2 D^d, and beta-2-microglobulin, while NB-V cells were negative to all three antigens. It was found that dimethyl sulfoxide (DMSO) had a capacity to increase an H-2 class I antigen expression on NB-1 cells, whereas no change was observed on NB-V cells after DMSO treatment. Molecular analysis with deoxyribonucleic and ribonucleic acid (RNA) blot hybridization and immunoprecipitation revealed that the enhancement of H-2 antigen expression on NB-1 cells was modulated at the transcriptional control of the H-2 gene. In contrast, negative H-2 antigen expression on NB-V cells was caused by block at the level of glycosylation of the H-2 heavy chain, although an increase in messenger RNA of the H-2 gene was induced after DMSO treatment. There was neither amplification nor rearrangement of N-myc and c-src oncogenes in either neuroblastoma subline. Nuclear runon transcription assay revealed that the N-myc gene was post-transcriptionally down-modulated by DMSO, whereas the c-src gene was transcriptionally up-regulated. It was thus suspected that N-myc and c-src might be directly associated with cellular proliferation and differentiation in neuronal tumors and that in vivo tumorigenicity could be regulated by the control mechanism of oncogene expression in relation to H-2 gene expression on tumor cells.
社団法人日本脳神経外科学会の論文
1990-11-01

神経芽細胞腫における癌遺伝子とMHC抗原遺伝子間の発現調節機構に関する検討 : マウス神経芽細胞腫を用いたH-2 Gene, N-myc, c-src相互間制御の分子生物学的解析

スポンサーリンク

概要

著者

関連論文

スポンサーリンク