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首页> 外文期刊>Life sciences >Reciprocal effects of NNK and SLURP-1 on oncogene expression in target epithelial cells.
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Reciprocal effects of NNK and SLURP-1 on oncogene expression in target epithelial cells.

机译：NNK和SLURP-1对靶标上皮细胞癌基因表达的相互影响。

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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：为了阐明烟草亚硝胺（4-（甲基亚硝胺基）-1-（3-吡啶基）-1-丁酮）（NNK）靶向的支气管和口腔上皮细胞上的烟碱乙酰胆碱受体如何促进致癌性转化。可以被烟碱能分泌的哺乳动物Ly-6 /尿激酶纤溶酶原激活物受体相关蛋白1（SLURP-1）废除，我们比较了NNK和重组（r）SLURP-1对永生化人类肿瘤发生相关基因表达的影响NNK分别刺激BEP2D中的MYB和PIK3CA，Het-1A中的ETS1，NRAS和SRC，以及两种细胞类型中的AKT1，KIT和RB1等致癌基因的表达。在存在rSLURP-1时可以取消。 rSLURP-1可以消除NNK上调的其他与癌症相关的基因是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（仅适用于Het-1A）。 NNK还上调了抗凋亡的BCL2（Het-1A），下调了促凋亡的TNF（Het-1A），BAX和CASP8（BEP2D），所有这些都可以部分被rSLURP-1废除。 NNK降低了编码细胞间粘附分子β-catenin（BEP2D）的CTNNB1基因的表达，并降低了BEP2D细胞中的肿瘤抑制因子CDKN3和FOXD3以及Het-1A细胞中的SERPINB5的表达。 rSLURP-1消除了NNK的这些致癌作用，rSLURP-1也上调了RUNX3的表达。细胞。

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