Identification of drug-resistance related genes in natural killer/T cell lymphoma through digital gene expression and RNA-sequencing

2017 
Objective To explore the differentially expressed genes among normal natural killer (NK) cell and NK/T cell lymphoma cell lines YTS and SNK-6 and define the expression of common drug-resistance related genes in NK/T cell lymphoma cell lines. Methods The digital gene expression (DGE) profiles of normal NK cells and NK/T-cell lymphoma cells YTS and SNK-6 were detected by DGE sequencing technology. The differential expressed genes among the three cell lines were also analyzed.3 184 genes were upregulated and 2 764 genes were downregulated in SNK-6 cells as compared with normal NK cells.3 978 genes were upregulated and 2 172 genes were downregulated in YTS cells as compared with normal NK cells. However, as compared with YTS cells, 1 068 genes were upregulated and 2 425 genes were downregulated in SNK-6 cells. The expression levels of common drug-resistance related genes were examined by real-time fluorescent quantitative polymerase chain reaction (FQ-PCR). Consequently, the DGE profiles of normal NK cells and two NK/T cell lymphoma cell lines were established. Results DGE libraries of one normal NK cell line and two NK/T cell lymphoma cell lines were established and significantly differentially expressed genes of three cell lines were screened. The level of multidrug resistance protein 5 (ABCC5) mRNA was significantly higher in both YTS cells (3.69±0.11, P=0.001) and SNK-6 cells (5.22±1.66, P=0.048) than in normal NK cells (1.00±0.00). The level of erythroblastic leukemia viral oncogene homolog 4 (ERBB4) mRNA was significantly higher in both YTS cells (6.87±0.56, P=0.003) and SNK-6 cells (14.79±1.84, P=0.006) than in normal NK cells (1.00±0.00). Conclusion The highly expressed ABCC5 and ERBB4 may be associated with drug resistance in NK/T cell lymphoma. We can foresee that drug-resistance related genes might be targets for detection and treatment of NK/T cell lymphoma patients. Key words: Drug resistance genes; Digital gene expression; Natural killer/T cell lymphoma
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