Department of Cardiothoracic Surgery, Tianjin Medical University General Hospital Tianjin, China.
Thorac Cancer. 2015 Nov;6(6):778-84. doi: 10.1111/1759-7714.12283. Epub 2015 Jun 23.
Micro ribonucleic acid (miR-101) can regulate the expression of cyclooxygenase-2 (COX-2) and participate in the pathogenesis of malignant tumors. This study investigates the effects of miRNA-101 and COX-2 in lung cancer and the impact of miR-101 on the proliferation and invasion of human lung cancer A549 cell line.
The expression of miR-101 in 20 separate lung cancer tissues was detected by real time polymerase chain reaction; COX-2 expression was also detected. A549 cells were transfected with miR-101 or negative control oligonucleotide duplex mimic (miR-NC). In vivo tumorigenesis abilities were detected in localized human lung cancer xeno-transplant models in BALB/c nude mice.
MiR-101 expression was significantly lower and the level of COX-2 significantly higher in lung cancer tissues than in adjacent parenchyma (2.918 ± 1.006 vs. 5.953 ± 1.976, P = 0.001; 0.887 ± 0.260 vs. 0.355 ± 0.156, P = 0.001, respectively). Correlation analysis revealed that miR-101 negatively correlated with COX-2 in lung cancer tissues (R = -0.596, P = 0.002). Compared with A549-miR-NC cells, the expression of COX-2 was significantly decreased in A549 cells transfected with miR-101 (P < 0.001). The proliferation of A549 cells was markedly inhibited after transfection of miR-101. The in vivo tumor growth of A549 cells transfected with miR-101 was significantly slower than wide type A549 cells.
MiR-101 expression is decreased in lung cancer, inducing an increase in COX-2 level. Enforced expression of miR-101 can remarkably reduce the cell proliferation and invasion ability of lung cancer cells.
微小核糖核酸(miR-101)可以调节环氧化酶-2(COX-2)的表达,并参与恶性肿瘤的发病机制。本研究探讨了 miR-101 和 COX-2 在肺癌中的作用,以及 miR-101 对人肺癌 A549 细胞系增殖和侵袭的影响。
采用实时聚合酶链反应检测 20 例肺癌组织中 miR-101 的表达,同时检测 COX-2 的表达。用 miR-101 或阴性对照寡核苷酸双工模拟物(miR-NC)转染 A549 细胞。在 BALB/c 裸鼠局部人肺癌异种移植模型中检测体内肿瘤生成能力。
肺癌组织中 miR-101 的表达明显低于癌旁实质组织,COX-2 的水平明显高于癌旁实质组织(2.918±1.006 比 5.953±1.976,P=0.001;0.887±0.260 比 0.355±0.156,P=0.001)。相关性分析显示,肺癌组织中 miR-101 与 COX-2 呈负相关(R=-0.596,P=0.002)。与 A549-miR-NC 细胞相比,转染 miR-101 的 A549 细胞中 COX-2 的表达明显降低(P<0.001)。转染 miR-101 后 A549 细胞的增殖明显受到抑制。转染 miR-101 的 A549 细胞的体内肿瘤生长明显慢于野生型 A549 细胞。
miR-101 在肺癌中表达下调,导致 COX-2 水平升高。过表达 miR-101 可显著降低肺癌细胞的增殖和侵袭能力。