• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Reciprocal effects of NNK and SLURP-1 on oncogene expression in target epithelial cells.
【24h】

Reciprocal effects of NNK and SLURP-1 on oncogene expression in target epithelial cells.

机译：NNK和SLURP-1对靶上皮细胞癌基因表达的互敏作用。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

To elucidate how the nicotinic acetylcholine receptors expressed on bronchial and oral epithelial cells targeted by the tobacco nitrosamine (4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone) (NNK) facilitate carcinogenic transformation.Since NNK-dependent transformation can be abolished by the nicotinergic secreted mammalian Ly-6/urokinase plasminogen activator receptor related protein-1 (SLURP-1), we compared effects of NNK and recombinant (r)SLURP-1 on the expression of genes related to tumorigenesis in human immortalized bronchial and oral epithelial cell lines BEP2D and Het-1A, respectively.NNK stimulated expression of oncogenic genes, including MYB and PIK3CA in BEP2D, ETS1, NRAS and SRC in Het-1A, and AKT1, KIT and RB1 in both cell types, which could be abolished in the presence of rSLURP-1. Other cancer-related genes whose upregulation by NNK was abolishable by rSLURP-1 were the growth factors EGF in BEP2D cells and HGF in Het-1A cells, and the transcription factors CDKN2A and STAT3 (Het-1A only). NNK also upregulated the anti-apoptotic BCL2 (Het-1A) and downregulated the pro-apoptotic TNF (Het-1A), BAX and CASP8 (BEP2D), all of which could be abolished, in part, by rSLURP-1. NNK decreased expression of the CTNNB1 gene encoding the intercellular adhesion molecule β-catenin (BEP2D), as well as tumor suppressors CDKN3 and FOXD3 in BEP2D cells and SERPINB5 in Het-1A cells. These pro-oncogenic effects of NNK were abolished by rSLURP-1 that also upregulated RUNX3.The obtained results identified target genes for both NNK and SLURP-1 and shed light on the molecular mechanism of their reciprocal effects on tumorigenic transformation of bronchial and oral epithelial cells.
机译：阐明如何在烟草亚硝基胺（4-（甲基亚氨基氨基氨基）-1-（3-吡啶基）-1-丁酮）（NNK）靶向的支气管和口腔上皮细胞上表达的烟碱乙酰胆碱受体如何促进致癌转化。依赖NNK依赖性转化可以通过烟碱分泌哺乳动物Ly的-6 /尿激酶纤溶酶原激活受体相关蛋白-1（SLURP-1）中，我们比较NNK和重组（r）的效果SLURP-1对人相关肿瘤发生的基因的表达永生化被废除支气管和口腔上皮细胞系BEP2D和HET-1A分别。NNK刺激了致癌基因的表达，包括在HET-1A的BEP2D，ETS1，NRAS和SRC中的MYB和PIK3CA，以及两种细胞类型中的AKT1，试剂盒和RB1可以在RSLURP-1的存在下被废除。其他癌症相关的基因，其上调的NNK可取消通过RSLURP-1是BEP2D细胞中的生长因子EGF和HET-1A细胞中的HGF，以及转录因子CDKN2A和STAT3（仅限HET-1A）。 NNK还上调抗凋亡BCL2（HET-1A），并下调促凋亡TNF（HET-1A），BAX和CASP8（BEP2D），所有这些都可以部分地由RSLURP-1被废除。 NNK降低了编码细胞间粘附分子β-连环蛋白（BEP2D）的CTNNB1基因的表达，以及肿瘤抑制剂CDKN3和FOXD3在BEP2D细胞中的HET-1A细胞中的SerpinB5。通过RSLURP-1废除了NNK的这些促致致癌作用，所述RSLURP-1也被上调的润荷荷丝3.得到的结果鉴定了NNK和SLURP-1的靶基因，并脱光对其对支气管和口腔上皮的致致瘤转化的致致瘤转化的分子机制细胞。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号