Objective : To explore the role of long non⁃coding RNA PITPNA⁃AS1 in ovarian cancer and its possible molecular mechanism. Methods : Fluorescence real⁃time quantitative polymerase chain reaction (qPCR) technology was used to detect the expression level of PITPNA⁃AS1 in ovarian cancer tissues and corresponding adjacent tissues , ovarian cancer cell lines and normal ovarian epithelial cell lines. The cell lines with the least expression of PITPNA⁃AS1 were divided into control group and experimental group , and transfected with negative control plasmid or PITPNA⁃AS1 plasmid respectively. Cell counting ( CCK⁃8) method and Transwell method were used to detect cell proliferation activity and invasion ability. Bioinformatics methods and dual luciferase activity reporter gene experiments predicted and verified the molecular mechanism of PITPNA⁃AS1 . qPCR and Western blot were used to detect the gene expression of PITPNA⁃AS1 interaction. Results : The expression of PITPNA⁃AS1 in ovarian cancer tissues was lower than that in adjacent tissues (P < 0. 01) . The expression level of PITPNA⁃AS1 in ovarian cancer cell lines was lower than that in normal ovarian epithelial cells (P < 0. 05) , and the expression in OVCAR⁃3 cells was the least (P < 0. 01) . Compared with the control group , overexpression of PITPNA⁃AS1 could inhibit the proliferation activity (P < 0. 05) and invasion ability (P < 0. 01) of OVCAR⁃3 cells. PITPNA⁃AS1 had a targeting relationship with miR⁃92a⁃3p (P < 0. 01) , and miR⁃92a⁃3p had a targeting relationship with transcription factor 21 (TCF21) ( P < 0. 01) . Overexpression of PITPNA⁃AS1 caused a decrease in the expression of miR⁃92a⁃3p in OVCAR⁃3 cells (P < 0. 01) , and an increase in the expression of TCF21 gene (P < 0. 01) . Conclusion PITP⁃NA⁃AS1 is lowly expressed in ovarian cancer tissues and cell lines. PITPNA⁃AS1 can inhibit the proliferation and invasion of ovarian cancer OVCAR⁃3 cells through targeted regulation of miR⁃92a⁃3p/TCF21 .

[摘 要] 目的：探讨lncRNA ZNF674-AS1在宫颈癌中的作用及其分子机制。方法：用qPCR法检测ZNF674-AS1在31例2019年1月至2020年7月在武汉儿童医院接受手术治疗患者的宫颈癌组织和对应的癌旁组织、宫颈癌细胞系（SiHa、HeLa、C33A和HCC94）和永生化子宫颈上皮细胞系中的表达。转染过表达ZNF674-AS1质粒及其阴性对照质粒至ZNF674-AS1表达最少的HCC94细胞，CCK-8法和Transwell实验检测过表达ZNF674-AS1对HCC94细胞增殖活性和迁移能力的影响。生物信息学方法预测和双荧光素酶报告基因实验验证ZNF674-AS1和miR-510-5p、REPS2三者间的互补结合关系。qPCR检测过表达ZNF674-AS1对miR-510-5p与REPS2表达的影响，WB法检测过表达ZNF674-AS对细胞增殖和迁移相关因子表达的影响。结果：与癌旁组织相比，ZNF674-AS1在宫颈癌组织中呈明显低表达（P<0.01）；与永生化子宫上皮细胞相比，ZNF674-AS1在宫颈癌细胞系中也呈明显低表达（P<0.05或P<0.01），以HCC94细胞中表达最低（P<0.01）。过表达ZNF674-AS1能明显抑制HCC94细胞的增殖（P<0.05）和迁移（P<0.01）。与ZNF674-AS1相互作用的miRNA是miR-510-5p，与miR-510-5p相互作用的基因是REPS2。过表达ZNF674-AS1导致HCC94细胞中miR-510-5p的表达水平降低（P<0.01）而REPS2基因的表达水平升高（P<0.01），同时引起细胞增殖和迁移相关的多种因子（CDK2、cyclin D3、vimentin和twist）上调或下调。结论：lncRNA ZNF674-AS1在宫颈癌组织和细胞中呈低表达，可能通过竞争性结合miR-510-5p而上调REPS2的表达，从而抑制宫颈癌HCC94细胞的增殖和迁移。