Background and purpose: Natural killer/T cell lymphoma in poor effects, the production of multidrug resistance is one of the reasons to reduce the chemotherapy effect or failure. This study aimed to discuss the multidrug resistance associated protein 4 (ABCC4/MRP4) gene and multidrug resistance associated protein 5 (ABCC5/MRP5) gene expression in NK/T cell lymphoma SNK-6, YTS cell lines and NK/T cell lymphoma tissues, and the relationship between the level of ABCC4/MRP4, ABCC5/MRP5 gene expression and the clinical efifcacy. Methods:Real-time lfuorescence quantitative PCR (Real time-PCR) and immunohistochemical method (IHC) were used to detect the ABCC4/MRP4, ABCC5/MRP5 gene and protein expression. Results:Compared with the normal NK cells, ABCC4/MRP4 and ABCC5/MRP5 gene in SNK-6, YTS cell lines were highly expressed (P<0.05); Compared with rhinitis tissues, the expression of ABCC4/MRP4, ABCC5/MRP5 gene was higher in the NK/T cell lymphoma tissues (P<0.05);The expression level of ABCC4/MRP4 and ABCC5/MRP5 gene was negative correlation with clinical efifcacy (P<0.05). Conclusion: The expression of ABCC4/MRP4 and ABCC5/MRP5 gene affects the of clinical efifcacy of NK/T cell lymphoma.

ObjectiveTo observe the effect of Guben Jiedu prescription （GBJ） on the epithelial-mesenchymal transition （EMT） of lung cancer A549 cells and to explore the mechanism based on phosphoinositide 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway. MethodThe GBJ-medicated serum was prepared. Cell viability was detected by methyl thiazolyl tetrazolium （MTT） assay to screen the optimal doses of GBJ-medicated serum for further experiment. A549 cells were classified into normal serum group， low-， medium-， and high-dose GBJ-medicated serum groups （2.5%， 5%， and 10% GBJ-medicated serum）， PI3K/Akt pathway activator SC79 group， and high-dose GBJ-medicated serum + SC79 group. Cell migration ability was measured by wound-healing assay. The protein expression of E-cadherin， N-cadherin， vimentin， Akt， phosphorylated Akt （p-Akt）， glycogen synthase kinase-3β （GSK-3β）， and phosphorylated GSK-3β （p-GSK-3β） was detected by Western blotting， and the mRNA expression of N-cadherin and vimentin by Real-time PCR. ResultCompared with the normal serum， GBJ-medicated serum （2.5%， 5%， 10%， 20%， 40%） decreased the viability of A549 cells （P<0.05）， and 10%， 5%， 2.5% GBJ-medicated serum was respectively selected for the follow-up experiment. The migration ability of cells in the high-， medium-， and low-dose GBJ-medicated serum groups was lower than that in the normal serum group. The expression of N-cadherin mRNA and Vimentin mRNA in A549 cells in the three GBJ-medicated serum groups was significantly lower than that in the normal serum group （P<0.01）. The protein expression of E-cadherin was higher in the high- and medium-dose GBJ-medicated serum groups than in the normal serum group （P<0.01）. The three GBJ-medicated serum groups showed lower protein expression of N-cadherin， vimentin， p-Akt， and p-GSK-3β （P<0.01） and lower expression of p-Akt/Akt， p-GSK-3β/GSK-3β （P<0.05， P<0.01） than normal serum group. Compared with the SC79 group， the high-dose GBJ-medicated serum group demonstrated high protein expression of E-cadherin （P<0.01） and low expression of N-cadherin， vimentin， p-Akt， p-GSK-3β， and p-Akt/Akt， p-GSK-3β/GSK-3β （P<0.01）. Compared with the high-dose GBJ-medicated serum group， high-dose GBJ-medicated serum + SC79 group showed low protein expression of E-cadherin （P<0.01） and high protein expression of N-cadherin， vimentin， p-Akt， p-GSK-3β， p-Akt/Akt， and p-GSK-3β/GSK-3β （P<0.01）. ConclusionGBJ can inhibit the migration and EMT of lung cancer A549 cells by regulating the PI3K/Akt signaling pathway.