CAJ | 학술논문

目的:利用RNA干扰(RNAi)技术沉默卵巢癌细胞系CAOV3细胞中诱骗受体 3 (DcR3)基因的表达,并探讨其对卵巢上皮性腺癌(卵巢癌)细胞增殖能力的影响.方法:构建DcR3 siRNA,并转染至卵巢癌CAOV3细胞中, 在细胞内被识别并降解CAOV3细胞中的DcR3 mRNA. 实验分为3组:DcR3 siRNA组、空白对照组和非特异性 siRNA 组(阴性对照组). 通过实时荧光定量(Real-time PCR, RT-PCR)检测 DcR3 mRNA表达水平的变化. 利用MTT实验观察DcR3 siRNA对卵巢癌细胞株CAOV3增殖能力的影响. 结果:DcR3 siRNA组细胞中DcR3 mRNA 的表达水平明显降低,与非特异性siRNA组及空白对照组相比,差异有显著性 (P < 0.05). 转染DcR3 siRNA的细胞增殖能力明显下降,与非特异性siRNA组及空白对照组相比,差异有统计学意义(P < 0.01). 结论:DcR3 siRNA能在细胞内被识别并降解CAOV3细胞中的DcR3 mRNA,从而发挥抑制卵巢癌细胞增殖的能力.
목적:이용RNA간우(RNAi)기술침묵란소암세포계CAOV3세포중유편수체 3 (DcR3)기인적표체,병탐토기대란소상피성선암(란소암)세포증식능력적영향.방법:구건DcR3 siRNA,병전염지란소암CAOV3세포중, 재세포내피식별병강해CAOV3세포중적DcR3 mRNA. 실험분위3조:DcR3 siRNA조、공백대조조화비특이성 siRNA 조(음성대조조). 통과실시형광정량(Real-time PCR, RT-PCR)검측 DcR3 mRNA표체수평적변화. 이용MTT실험관찰DcR3 siRNA대란소암세포주CAOV3증식능력적영향. 결과:DcR3 siRNA조세포중DcR3 mRNA 적표체수평명현강저,여비특이성siRNA조급공백대조조상비,차이유현저성 (P < 0.05). 전염DcR3 siRNA적세포증식능력명현하강,여비특이성siRNA조급공백대조조상비,차이유통계학의의(P < 0.01). 결론:DcR3 siRNA능재세포내피식별병강해CAOV3세포중적DcR3 mRNA,종이발휘억제란소암세포증식적능력.
Objective To investigate the effects of siRNA targeting decoy receptor 3 on the cell proliferation of ovarian carcinoma cell CAOV3. Methods We constructed siRNA targeting decoy receptor 3,which was transfected into ovarian carcinoma cells CAOV3 , and observed the effects of DcR3 siRNA on the cell proliferation of CAOV3 cell by MTT experiment. The experiment contained 3 groups, including the normal control group (CAOV3 cell was not transfected), the negative control group (CAOV3 cell was transfected with blank vector) and the experimental group (CAOV3 cell was transfected with DcR3 siRNA). The expression levels of DcR3 mRNA were detected by Real-time PCR. Results DcR3 siRNA recognized and degraded DcR3 mRNA in CAOV3 cells of the experimental group. DcR3 mRNA of the experimental group was significantly decreased. The proliferation of CAOV3 cell was significantly decreased by DcR3 siRNA comparing with the normal control group and negative control group (P < 0.01). Conclusion DcR3 siRNA can inhibit the proliferation of ovarian cancer cell line CAOV3 by recognized and degraded DcR3 mRNA.