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目的:探讨长链非编码RNA(lncRNA)DLG1反义RNA 1(DLG1-AS1)对结直肠癌细胞增殖、凋亡的影响和潜在分子机制。方法:2019年7月至2020年3月，结直肠癌细胞(SW620、Caco-2、SW480)和正常结肠上皮细胞(NCM460)购自美国模式培养物保藏中心。实时定量反转录聚合酶链反应(RT-qPCR)检测DLG1-AS1和微小RNA(miRNA，miR)-1305表达在结直肠癌细胞(SW620、Caco-2、SW480)和正常结肠上皮细胞(NCM460)中的表达。将DLG1-AS1小干扰RNA、miR-1305模拟物分别转染SW620细胞，细胞计数试剂盒、流式细胞术分别检测干扰DLG1-AS1或过表达miR-1305对SW620细胞活力、凋亡的影响。双荧光素酶报告基因实验和RT-qPCR确定DLG1-AS1对miR-1305的靶向调控作用。采用n t检验评估两组之间的差异，采用单因素方差分析和LSD-n t检验比较多组间的差异。n 结果:与NCM460细胞比较，SW620、Caco-2、SW480细胞中DLG1-AS1表达显著升高(3.68±0.24比1.00±0.05，1.93±0.18比1.00±0.05，2.62±0.21比1.00±0.05，n t＝32.796、14.935、22.514，n P<0.05)，miR-1305表达显著降低(0.42±0.04比1.00±0.07，0.57±0.05比1.00±0.07，0.36±0.03比1.00±0.07，n t＝21.582、14.996、25.211，n P<0.05)。干扰DLG1-AS1表达后SW620细胞活力显著降低(0.51±0.04比0.99±0.06，n t＝19.969，n P<0.05)，细胞凋亡率显著升高(23.11±2.33比7.49±0.69，n t＝19.284，n P<0.05)。过表达miR-1305后SW620细胞活力显著降低(0.63±0.06比0.97±0.05，n t＝13.060，n P<0.05)，细胞凋亡率显著升高(17.99±1.60比7.78±0.72，n t＝17.458，n P<0.05)。miR-1305是DLG1-AS1的靶基因，DLG1-AS1负调控miR-1305表达。抑制miR-1305表达能够逆转干扰DLG1-AS1对SW620细胞活力(0.87±0.07比0.49±0.03，n t＝14.969，n P<0.05)、凋亡(13.63±1.22比24.16±2.49，n t＝11.393，n P<0.05)的影响。n 结论:干扰DLG1-AS1通过上调miR-1305可抑制结直肠癌细胞增殖、诱导细胞凋亡。“,”Objective:To explore the effect of long-chain non-coding RNA (lncRNA) DLG1 antisense RNA 1 (DLG1-AS1) on proliferation and apoptosis of colorectal cancer cells and its potential molecular mechanism.Methods:The study was completed between July 2019 and March 2020. Colorectal cancer cells (SW620, Caco-2, SW480) and normal colonic epithelial cells (NCM460) were purchased from the American Type Culture Collection.Real-time quantitative reverse transcriptase-polymerase chain reaction (RT-qPCR) was used to detect the expression of DLG1-AS1 and microRNA (miRNA, miR)-1305 in colorectal cancer cells (SW620, Caco-2, SW480) and normal colon epithelial cells (NCM460). The DLG1-AS1 small interfering RNA and miR-1305 mimic were transfected into SW620 cells, respectively. The cell counting kit and flow cytometry were used to detect the effect of interfering with DLG1-AS1 or overexpressing miR-1305 on SW620 cell viability and apoptosis. The dual luciferase reporter gene experiment and RT-qPCR confirmed the targeted regulation between miR-1305 and DLG1-AS1. the n t test was used to evaluate the difference between the two groups, and the one-way analysis of variance and LSD-n t test were used to compare the differences between multiple groups.n Results:Compared with NCM460 cells, the expression of DLG1-AS1 in SW620, Caco-2, and SW480 cells was significantly increased (3.68±0.24 vs. 1.00±0.05, 1.93±0.18 vs. 1.00±0.05, 2.62±0.21 vs. 1.00±0.05, n t=32.796, 14.935, 22.514, n P<0.05), while the expression of miR-1305 was significantly decreased (0.42±0.04 vs. 1.00±0.07, 0.57±0.05 vs. 1.00±0.07, 0.36±0.03 vs. 1.00±0.07,n t=21.582, 14.996, 25.211, n P<0.05). After interfering with the expression of DLG1-AS1, the vitality of SW620 cells was significantly reduced (0.51±0.04 vs. 0.99±0.06,n t=19.969, n P<0.05), and the apoptosis rate was significantly increased (23.11±2.33 vs. 7.49±0.69,n t=19.284, n P<0.05). After overexpression of miR-1305, the viability of SW620 cells was significantly reduced (0.63±0.06 vs. 0.97±0.05,n t=13.060, n P<0.05), and the apoptosis rate was significantly increased (17.99±1.60 vs. 7.78±0.72,n t=17.458, n P<0.05). miR-1305 is the target gene of DLG1-AS1, and DLG1-AS1 negatively regulates miR-1305 expression. Inhibition of miR-1305 expression could reverse the effect of interfering with DLG1-AS1 on the vitality (0.87±0.07 vs. 0.49±0.03,n t=14.969, n P<0.05) and apoptosis (13.63±1.22 vs. 24.16±2.49,n t=11.393, n P<0.05) of SW620 cells.n Conclusion:Interfering with DLG1-AS1 could inhibit the proliferation and induce apoptosis of colorectal cancer cells by up-regulating miR-1305.