【摘要】 目的:探讨miR-199b-5p在2型乳头状肾细胞癌(PRCC)合并下腔静脉瘤栓患者中的表达及其功能。方法:应用miRNA芯片检测2型PRCC合并及不合并下腔静脉瘤栓各10例患者的miRNA差异表达谱。应用RT-qPCR在22对样本中对差异表达的候选基因进行扩大样本验证。使用miR-199b-5p的过表达质粒(miR-199b-5p-up)和阴性对照质粒(NC)分别转染CAKI-2和CAL-54细胞,检测2组细胞的增殖及侵袭能力变化情况,细胞增殖抗原(Ki67)和基质金属蛋白酶2(MMP2)的表达。结果:与不合并下腔静脉瘤栓的2型PRCC组织样本相比,合并瘤栓的癌组织中miR-199b-5p显著下调(P<0.05)。与NC组相比,miR-199b-5p-up组CAKI-2和CAL-54细胞的增殖和侵袭能力均降低(P<0.05)。对照组和合并下腔静脉瘤栓组的癌组织样本中,Ki67和MMP2表达分别显著高于miR-199b-5p-up组和不合并下腔静脉瘤栓组(均P<0.05)。结论:肾癌中miR-199b-5p下调可能通过调控Ki67和MMP2介导2型PRCC下腔静脉瘤栓的形成。更多还原

【Abstract】 Objective:To investigate the expression and function of miR-199 b-5 p in type 2 papillary renal cell carcinoma(PRCC)with inferior vena cava tumor thrombus.Methods:The miRNA chip was used to detect the miRNA differential expression profile of 10 pairs of type 2 PRCC with and without inferior vena cava tumor thrombus.RT-qPCR was used to expand the sample to verify the differentially expressed candidate genes in 22 pairs of samples.CAKI-2 and CAL-54 cells were transfected with miR-199 b-5 p overexpression plasmid(miR-199 b-5 p-up)and negative control plasmid(NC),respectively.Both groups were detected by CCK-8 method and cell invasion experiment for the changes in cell proliferation and invasion ability,and RT-qPCR was used to detect the expression of cell proliferation antigen(Ki67)and matrix metalloproteinase 2(MMP2)of cell samples and clinical samples.Results:Compared with type 2 PRCC tissue samples without inferior vena cava tumor thrombi,miR-199 b-5 p was significantly down-regulated in cancer tissues with tumor thrombi(P<0.05).Compared with the NC group,the proliferation and invasion abilities of CAKI-2 and CAL-54 cells in the miR-199 b-5 p-up group were reduced(P<0.05).RT-qPCR results showed that the expressions of Ki67 and MMP2 in the cancer tissue samples of the NC group and the inferior vena cava tumor thrombus group were significantly higher than those in the miR-199 b-5 p-up group and the group without inferior vena cava tumor thrombus.Conclusion:In type 2 PRCC,miR-199 b-5 p is down-regulated and it may mediate the formation of inferior vena cava tumor thrombus in renal cell carcinoma by regulating Ki67 and MMP2.更多还原