CAJ | 학술논문

目的观察Notch信号抑制剂(2S)-N-N-(3,5-氟苯乙酰基)-L-丙氨酰-2-苯基甘氨酸叔丁酯(DAPT)对肾小管上皮细胞HKC及肾肿瘤细胞786-O中c-myc表达及对细胞增殖的影响.方法通过实时定量聚合酶链反应(real-time PCR)及Western blot方法连续3次检测HKC及786-O 中c-myc的表达及DAPT处理后HKC及786-O细胞中c-myc的表达变化,并检测DAPT对细胞增殖及周期的影响.结果 786-O中c-myc表达比HKC高(2.54±0.24)倍(P＜0.01).DAPT处理后,HKC及786-O细胞中c-myc表达分别下调(1.41±0.13)和(2.93±0.26)倍(P均＜0.05)；两株细胞的增殖均受到抑制,HKC及786-O G0/G1期细胞比例分别增加9.75％和16.54％(P均＜0.01).结论 Notch信号抑制剂DAPT可能通过抑制c-myc的表达而抑制肾正常及肿瘤细胞的增殖.
목적 관찰Notch신호억제제(2S)-N-N-(3,5-불분을선기)-L-병안선-2-분기감안산숙정지(DAPT)대신소관상피세포HKC급신종류세포786-O중c-myc표체급대세포증식적영향.방법 통과실시정량취합매련반응(real-time PCR)급Western blot방법련속3차검측HKC급786-O 중c-myc적표체급DAPT처리후HKC급786-O세포중c-myc적표체변화,병검측DAPT대세포증식급주기적영향.결과 786-O중c-myc표체비HKC고(2.54±0.24)배(P＜0.01).DAPT처리후,HKC급786-O세포중c-myc표체분별하조(1.41±0.13)화(2.93±0.26)배(P균＜0.05)；량주세포적증식균수도억제,HKC급786-O G0/G1기세포비례분별증가9.75％화16.54％(P균＜0.01).결론 Notch신호억제제DAPT가능통과억제c-myc적표체이억제신정상급종류세포적증식.
Objective To investigate the contribution of Notch signaling inhibitor N-[ N-(3,5-di-fluorophenacetyl)-L-alanyl ]-S-phenylglycine t-butylester (DAPT) to c-myc expression and determine its functions in human kidney tubule epithelial cell line HKC and renal cell carcinoma (RCC) cell line 786-O.Methods Basal expression of c-myc in HKC and 786-O cells and that of c-myc in cells with or without DAPT treatments were detected by using triplicate real-time polymerase chain reaction (PCR) and Western blotting.Furthermore,proliferation and cell cycle assays were performed on these cells.Results c-myc was upregulated in 786-O cells relative to HKC (2.54 ±0.24 folds,P ＜0.01 ).After DAtT treatments,c-myc expression in 786-O and HKC cells were both downregulated (2.93 ±0.26 folds,and 1.41 ±0.13 folds,respectively,both P ＜ 0.05 ) ; Cell proliferation was attenuated and cell cycles were arrested at Go/G1 phase ( 16.54％ in 786-O cells and 9.75％ in HKC cells,respectively,both P ＜0.01 ).Conclusion Notch pathway signaling is associated with kidney normal and cancer cells proliferation and c-myc may serve as a target gene.