CAJ | 학술논문

背景与目的:NAG7基因是我室克隆的鼻咽癌相关的肿瘤抑制候选基因,其功能与作用机制目前尚不清楚.研究鼻咽癌相关的潜在抑瘤基因NAG7对鼻咽癌细胞系(HNE1)细胞周期和细胞凋亡的影响,并探讨其作用机制.方法:采用脂质体转染技术将NAG7基因导入HNE1细胞,建立稳定表达NAG7的细胞株,Northernblot分析转染细胞NAG7基因的表达,并采用流式细胞技术检测细胞周期、细胞周期素及细胞凋亡的改变,并用westernblot验证.结果:NAG7基因重表达的HNE1细胞与空载体转染的HNE1和HNE1细胞相比:G0/G1期细胞数增加(P<0.05),S期细胞数减少;细胞凋亡数目增加(P<0.05);细胞周期素A、D1、E表达明显降低(P<0.05),细胞周期素B1表达降低,Westernblot检测亦证实cyclinD1和cyclinE表达明显下调.结论:NAG7的重表达导致细胞周期素表达下调,从而延缓细胞经G1期进入S周期及诱导细胞凋亡增加进而抑制NPC细胞的过度增殖.
배경여목적:NAG7기인시아실극륭적비인암상관적종류억제후선기인,기공능여작용궤제목전상불청초.연구비인암상관적잠재억류기인NAG7대비인암세포계(HNE1)세포주기화세포조망적영향,병탐토기작용궤제.방법:채용지질체전염기술장NAG7기인도입HNE1세포,건립은정표체NAG7적세포주,Northernblot분석전염세포NAG7기인적표체,병채용류식세포기술검측세포주기、세포주기소급세포조망적개변,병용westernblot험증.결과:NAG7기인중표체적HNE1세포여공재체전염적HNE1화HNE1세포상비:G0/G1기세포수증가(P<0.05),S기세포수감소;세포조망수목증가(P<0.05);세포주기소A、D1、E표체명현강저(P<0.05),세포주기소B1표체강저,Westernblot검측역증실cyclinD1화cyclinE표체명현하조.결론:NAG7적중표체도치세포주기소표체하조,종이연완세포경G1기진입S주기급유도세포조망증가진이억제NPC세포적과도증식.
Background ＆ Objective: NPC associated gene NAG7 was a novel candidate tumor suppressor gene associated with nasopharyngeal carcinoma cloned in our laboratory. This study was designed to investigate the potential effect of NAG7 on the cell cycle and apoptosis of nasopharyngeal carcinoma cell line HNE1 and its molecular mechanism. Methods: NAG7 genegene was introduced into HNE1 cells using lipofectin transfection technique. The expression level of NAG7 gene was analyzed by Northern blot. Cell cycle, cyclins, and cell apoptosis were detected by flow cytometry, and the expressions of cyclin D1 and cyclin E were detected by Western blot. Results: NAG7 gene was re expressed in NAG7 transfected HNE1 cells. Compared with HNE1 cells and vector transfected HNE1 cells, NAG7 transfected HNE1 cells arrested in G0/G1 phase increased (P< 0.05) and cells in S phase decreased (P< 0.05), the apoptosis cells increased (P< 0.05), and the levels of cyclins of A, B1, D1, and E decreased. Furthermore, the expression of cyclin D1 and E decreased in NAG7 transfected HNE1 cells. Conclusion: NAG7 gene re expression could inhibit overproliferation of NPC cell by delaying the progression of G1 into S in cell cycle and inducing cell apoptosis.