Wang Weiwei, Shen Fujun, Wang Chunlei, Lu Wenying, Wei Jun, Shang Anquan, Wang Chunbin
1 Department of Pathology, The First People's Hospital of Yancheng City, Yancheng, China.
2 Department of Pathology, The Sixth People's Hospital of Yancheng City, Yancheng, China.
Tumour Biol. 2017 Jun;39(6):1010428317698383. doi: 10.1177/1010428317698383.
We attempted to analyze the effects of miR-1-3p and CCL2 on the proliferation, migration, and invasion of bladder cancer cells. A total of 18 pairs of bladder cancer tissues with corresponding adjacent tissues and the 6 cases of normal tissues were collected. The expressions of miR-1-3p and CCL2 in the cancer tissues were evaluated using quantitative real-time polymerase chain reaction and western blot. The relationship between miR-1-3p and CCL2 was assessed using luciferase reporter assay. The UM-UC-3 bladder cancer cells were transfected with CCL2 small interfering RNA and miR-1-3p mimics. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, colony formation assay, wound healing assay, Transwell assay, and the flow cytometry test were used to detect the proliferation, migration, invasion, and apoptosis of bladder cancer cells. Bladder cancer tissues had lower levels of miR-1-3p but higher levels of CCL2 than normal tissues ( p < 0.05). The transfection of miR-1-3p mimics and CCL2 small interfering RNA remarkably suppressed cell proliferation and invasion and promoted apoptosis of cells ( p < 0.05). Results of the luciferase reporter gene assay demonstrated that miR-1-3p targeted CCL2. MiR-1-3p suppresses the proliferation and invasion of urinary bladder cancer cells by targeting CCL2.
我们试图分析miR-1-3p和CCL2对膀胱癌细胞增殖、迁移和侵袭的影响。共收集了18对膀胱癌组织及其相应的癌旁组织以及6例正常组织。采用定量实时聚合酶链反应和蛋白质免疫印迹法评估癌组织中miR-1-3p和CCL2的表达。采用荧光素酶报告基因检测法评估miR-1-3p与CCL2之间的关系。用CCL2小干扰RNA和miR-1-3p模拟物转染UM-UC-3膀胱癌细胞。采用噻唑蓝比色法、集落形成试验、伤口愈合试验、Transwell试验和流式细胞术检测膀胱癌细胞的增殖、迁移、侵袭和凋亡。与正常组织相比,膀胱癌组织中miR-1-3p水平较低,但CCL2水平较高(p<0.05)。转染miR-1-3p模拟物和CCL2小干扰RNA可显著抑制细胞增殖和侵袭,并促进细胞凋亡(p<0.05)。荧光素酶报告基因检测结果表明,miR-1-3p靶向CCL2。miR-1-3p通过靶向CCL2抑制膀胱癌细胞的增殖和侵袭。