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目的探讨微小核糖核酸(microRNA,miR)-139-5p在结肠炎相关肿瘤(CAC)中的作用机制。方法选取SPF级雄性C57BL/6小鼠24只,随机分为miR-139-5p敲除型组(miR-139-5p基因敲除小鼠)和对照组(miR-139-5p基因野生型小鼠),各12只,建立CAC动物模型。观察两组结肠肿瘤生长情况,实时荧光定量PCR检测增殖细胞核抗原(PCNA)以及促炎因子mRNA相对表达量。结果 miR-139-5p敲除型组小鼠肿瘤数为(12.56±3.61)个,明显多于对照组(5.22±1.30)个(P<0.01);miR-139-5p敲除型组小鼠肿瘤直径为(3.51±0.82)mm,明显大于对照组的(2.03±0.96)mm(P<0.01);miR-139-5p敲除型组小鼠PCNA mRNA相对表达量为2.71±0.78,明显高于对照组的1.06±0.34(P<0.01);miR-139-5p敲除型组小鼠白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、环氧合酶2(COX2)和巨噬细胞炎性蛋白(MIP2)的mRNA相对表达量分别为1.65±0.71、2.13±0.84、6.56±1.24和7.06±1.16,明显高于对照组的0.93±0.43、1.08±0.75、1.22±0.43、1.20±0.57(P<0.05,P<0.01)。结论 miR-139-5p在CAC的发生过程中具有重要意义,具有抑制炎性因子表达、阻止肿瘤细胞过度增殖等作用。
Objective To investigate the mechanism of microRNA (miR) -139-5p in colitis-associated tumors (CAC). Methods Twenty-four male SPF C57BL / 6 mice were randomly divided into miR-139-5p knockout (miR-139-5p knockout) and control (miR-139-5p wild type Rats), 12 rats in each group. Animal models of CAC were established. The growth of colon cancer in both groups was observed. The expression of proliferating cell nuclear antigen (PCNA) and proinflammatory cytokine mRNA was detected by real-time fluorescence quantitative PCR. Results The number of tumor in miR-139-5p knockout mice was (12.56 ± 3.61), which was significantly higher than that in control group (5.22 ± 1.30) (P <0.01). MiR-139-5p knockout mice The tumor diameter was (3.51 ± 0.82) mm, which was significantly higher than that of the control group (2.03 ± 0.96) mm (P <0.01). The relative expression of PCNA mRNA in miR-139-5p knockout mice was 2.71 ± 0.78 (1.06 ± 0.34) in the control group (P <0.01). The levels of interleukin-6, tumor necrosis factor-α and cyclooxygenase 2 in the miR- COX2 and MIP2 were 1.65 ± 0.71, 2.13 ± 0.84, 6.56 ± 1.24 and 7.06 ± 1.16, respectively, which were significantly higher than that of the control group (0.93 ± 0.43,1.08 ± 0.75,1.22 ± 0.43,1.20 ± 0.57 (P <0.05, P <0.01). Conclusion miR-139-5p plays an important role in the pathogenesis of CAC. It inhibits the expression of inflammatory cytokines and prevents the excessive proliferation of tumor cells.