目的:探讨长链非编码RNA树突状细胞-特异性跨膜蛋白域包含1-反义链1(DCST1-AS1)结合α-烯醇化酶(ENO1)在三阴性乳腺癌细胞增殖和侵袭中的作用。方法:通过基因本体分析寻找DCST1-AS1的潜在靶标；通过癌症基因组图谱分析ENO1在乳腺癌中的表达和预后；采用RNA免疫沉淀实验、实时定量聚合酶链反应和蛋白质免疫印迹研究DCST1-AS1与ENO1之间的相互作用；采用细胞增殖实验和侵袭实验研究DCST1-AS1结合ENO1对细胞增殖和侵袭的影响。使用GraphPad Prism 8软件处理数据，组间比较采用配对n t检验。n 结果:基因本体分析表明DCST1-AS1下拉蛋白ENO1参与肿瘤能量代谢与细胞间黏附等重要生物过程。癌症基因组图谱显示ENO1在乳腺癌亚型中差异表达且与患者的不良预后明显相关(n P< 0.01)。干扰DCST1-AS1能显著下调ENO1 mRNA(0.45±0.01，n t＝11.815，n P< 0.01)，差异有统计学意义，而过表达DCST1-AS1则显著上调ENO1 mRNA(4.15±0.07，n t＝63.424，n P< 0.01)，差异有统计学意义。干扰ENO1表达不仅使过表达DCST1-AS1的MDA-MB-231细胞的增殖能力受损(小干扰RNA组吸光度值分别为0.68±0.10、0.95±0.06、1.58±0.10、1.91±0.15；小干扰RNA对照组吸光度值分别为0.83±0.16、1.60±0.18、2.51±0.17、2.82±0.13，n t＝3.641，n P< 0.05)，差异有统计学意义，还抑制了细胞的侵袭(siRNA组，1.00±0.57，siNC组，3.34±0.71，n t＝4.462，n P< 0.05)，差异有统计学意义。n 结论:DCST1-AS1通过调控ENO1促进三阴性乳腺癌的增殖和侵袭。“,”Objective:To explore the role of long non-coding RNA dendritic cell-specific transmembrane protein domain containing 1-antisense 1 (DCST1-AS1) combined with α-enolase (ENO1) in the proliferation and invasion of triple-negative breast cancer cells (TNBC).Methods:Gene Ontology (GO) analysis was used to find potential targets of DCST1-AS1. The Cancer Genome Atlas (TCGA) was used to analyze the expression and prognosis of ENO1 in breast cancer. RNA immunoprecipitation, real-time quantitative polymerase chain reaction and Western blotting were used to study the interactions between DCST1-AS1 and ENO1. Cell proliferation and invasion experiments were used to study the effects of DCST1-AS1 combined with ENO1 on cell proliferation and invasion. GraphPad Prism 8 software was used for data processing, and paired n t test was used for comparison between groups.n Results:GO analysis showed that the DCST1-AS1 pull-down protein ENO1 was involved in tumor energy metabolism and cell adhesion. TCGA analysis showed that ENO1 was differentially expressed in molecular subtypes of breast cancer and was related to poor prognosis of patients (n P< 0.01). Interference with DCST1-AS1 down-regulated ENO1 mRNA (0.45±0.01,n t=11.815, n P<0.01), while overexpression of DCST1-AS1 up-regulated ENO1 mRNA (4.15±0.07,n t=63.424, n P<0.01). Interfering with ENO1 expression not only significantly impaired the proliferation of MDA-MB-231 cells overexpressing DCST1-AS1 (The absorbance values of the small interfering RNA groups were 0.68±0.10, 0.95±0.06, 1.58±0.10, 1.91±0.15; and those of the small interfering RNA negative control groups were 0.83±0.16, 1.60±0.18, 2.51±0.17, 2.82±0.13,n t=3.641, n P<0.05), but also inhibited cell invasion (siRNA groups, 1.00±0.57; siNC groups, 3.34±0.71,n t=4.462, n P<0.05).n Conclusion:DCST1-AS1 promotes the proliferation and invasion of TNBC cells by regulating ENO1.