[摘要] 目的：探讨长链非编码RNA（long-chain non-coding RNA，lncRNA）TTTY10 对宫颈癌细胞迁移和侵袭的影响及其对miR-490-3p 及高迁移率族蛋白1（high mobility group box 1, HMGB1）信号通路的调控作用。方法：收集华中科技大学同济医学院附属武汉中心医院妇产科2013 年8 月至2014 年10 月14 例宫颈癌患者的癌组织及相对应的癌旁组织标本，qPCR检测宫颈癌组织及不同宫颈癌细胞株中TTTY10 表达情况。将编码TTTY10-siRNA 的质粒或空载质粒转染至宫颈癌CasKi 细胞中，qPCR检测质粒TTTY10-siRNA转染宫颈癌细胞的转染效率，Transwell 迁移和侵袭实验检测沉默TTTY10 后宫颈癌细胞迁移和侵袭能力的变化，qPCR检测沉默TTTY10 后miR-490-3p 和HMGB1 mRNA的表达。双荧光素酶报告基因检测miR-490-3p 与HMGB1 的相互作用，Western blotting 检测沉默TTTY10 后HMGB1 信号通路蛋白的表达情况。结果：宫颈癌组织中TTTY10 的表达显著高于癌旁组织，宫颈癌细胞株中TTTY10 的表达显著高于宫颈上皮永生化细胞（P<0.01）；TTTY10-siRNA 质粒可以有效转染进入CasKi细胞内并敲减TTTY10 的表达（P<0.01），沉默TTTY10 可以抑制宫颈癌CasKi 细胞的迁移和侵袭能力，促进宫颈癌细胞miR-490-3p 的表达和抑制HMGB1 mRNA的表达（P<0.05 或P<0.01）。miR-490-3p 能与HMGB1 mRNA的3′ -UTR特异性结合，沉默TTTY10后HMGB1 信号通路蛋白表达水平下调。结论：TTTY10 可以靶向调节miR-490-3p，并且通过HMGB1 信号通路影响宫颈癌CasKi细胞的迁移和侵袭能力；TTTY10 可作为宫颈癌的诊断标志物和潜在的药物治疗靶点。

[Abstract] Objective：To investigate the effect of long-chain non-coding RNA TTTY10 (lncRNA TTTY10) on the migration and invasion of cervical cancer cells, and to explore its regulatory effect on miR-490-3p and HMGB1 (high mobility group box 1) signaling pathways.Methods: Fourteen paris of cervical cancer tissues and corresponding paracancerous tissues resected at the Department of Obstetrics and Gynecology, Affiliated Wuhan Central Hospital of Tongji Medical College from August 2013 to December 2014 were collected for this study. The expression of TTTY10 in cervical cancer tissue and different cervical cancer cell lines were detected by qPCR. Plasmids encoding TTTY10-siRNA or empty plasmids were transfected into cervical cancer CasKicells, and the transfection efficiency was detected by qPCR. Transwell migration assay and Transwell invasion assay were used to detect the migration and invasion abilities of cervical cancer cells after TTTY10 silencing. qPCR was used to detect the expression of miR-490-3p and HMGB1 mRNA after TTTY10 silencing. Dual luciferase reporter assay validated the interaction between miR-490-3p and HMGB1. Western blotting was used to detect the expression of HMGB1 signaling pathway related proteins after TTTY10 silencing. Results: The expression of TTTY10 in cervical cancer tissues was significantly higher than that in paracancerous tissues (P<0.01), the expression of TTTY10 in cervical cancer cell lines was significantly higher than that in cervical epithelial cells (P<0.01). TTTY10-siRNA plasmids could efficiently transfect CasKicells to knockdown TTTY10 expression (P<0.01). Silencing of TTTY10 inhibited the migration and invasion of cervical cancer CasKi cells (P<0.05), promoted the expression of miR-490-3p (P<0.01) and inhibited the expression of HMGB1 mRNA in cervical cancer (P<0.05 or P<0.01). miR-490-3p could specifically bind to the 3'-UTR of HMGB1 mRNA (P<0.01). HMGB1 signaling pathway related proteins were down-regulated after TTTY10 silencing. Conclusion: TTTY10 can target regulate the expression of miR-490-3p and affect the migration and invasion ability of cervical cancer CasKi cells through the HMGB1 signaling pathway; TTTY10 can be used as a diagnostic marker and potential treatment target of cervical cancer.