Long noncoding RNAs (lncRNAs) are usually dysregulated in the progression of pancreatic cancer. This research aims to explore the function and mechanism of LINC00261 in pancreatic cancer cell viability, invasion and apoptosis. Cancer Genome Atlas (TCGA) database was applied to analyze the association between survival probability of patients and level of LINC00261 or miR-23a-3p in pancreatic cancer. Quantitative reverse transcription polymerase chain reaction was conducted to analyze the levels of LINC00261 and miR-23a-3p. Cell viability, invasion and apoptosis of pancreatic cancer cells were determined via MTT, transwell invasion assay, and flow cytometry, respectively. The target relationship between LINC00261 and miR-23a-3p was determined via dual-luciferase reporter and RNA immunoprecipitation assays. Low level of LINC00261 indicated low survival probability of pancreatic cancer patients. LINC00261 level was decreased in pancreatic cancer cells than that in normal pancreatic ductal epithelial cells. Addition of LINC00261 restrained cell viability and invasion and facilitated apoptosis. miR-23a-3p was negatively correlated with LINC00261 level and high expression of miR-23a-3p indicated low survival probability. miR-23a-3p was targeted by LINC00261 and attenuated the influence of LINC00261 on pancreatic cancer cell viability, invasion and apoptosis. In conclusion, LINC00261 overexpression repressed cell viability and invasion and enhanced apoptosis by decreasing miR-23a-3p expression in pancreatic cancer cells, indicating a new target for the treatment of pancreatic cancer.

长非编码RNA（lncRNA）通常在胰腺癌的进展中失调。本研究旨在探讨LINC00261在胰腺癌细胞存活，侵袭和凋亡中的功能和机制。应用癌症基因组图谱（TCGA）数据库分析了胰腺癌患者的生存概率与LINC00261或miR-23a-3p水平之间的关联。进行定量逆转录聚合酶链反应以分析LINC00261和miR-23a-3p的水平。分别通过MTT，穿孔侵袭测定和流式细胞术确定胰腺癌细胞的细胞存活力，侵袭和凋亡。LINC00261和miR-23a-3p之间的靶标关系通过双荧光素酶报告基因和RNA免疫沉淀测定法确定。LINC00261含量低表明胰腺癌患者的生存率低。胰腺癌细胞中的LINC00261水平低于正常胰腺导管上皮细胞中的LINC00261水平。LINC00261的加入抑制细胞活力和侵袭并促进细胞凋亡。miR-23a-3p与LINC00261水平呈负相关，miR-23a-3p的高表达表明其生存率较低。miR-23a-3p被LINC00261靶向，并减弱了LINC00261对胰腺癌细胞活力，侵袭和凋亡的影响。总之，LINC00261过表达通过降低胰腺癌细胞中miR-23a-3p的表达来抑制细胞活力和侵袭，并增强细胞凋亡，这是治疗胰腺癌的新靶点。胰腺癌细胞中的LINC00261水平低于正常胰腺导管上皮细胞中的LINC00261水平。LINC00261的加入抑制细胞活力和侵袭并促进细胞凋亡。miR-23a-3p与LINC00261水平呈负相关，而miR-23a-3p的高表达表明其生存率较低。miR-23a-3p被LINC00261靶向，并减弱了LINC00261对胰腺癌细胞活力，侵袭和凋亡的影响。总之，LINC00261过表达通过降低胰腺癌细胞中miR-23a-3p的表达来抑制细胞活力和侵袭，并增强细胞凋亡，这是治疗胰腺癌的新靶点。胰腺癌细胞中的LINC00261水平低于正常胰腺导管上皮细胞中的LINC00261水平。LINC00261的加入抑制细胞活力和侵袭并促进细胞凋亡。miR-23a-3p与LINC00261水平呈负相关，miR-23a-3p的高表达表明其生存率较低。miR-23a-3p被LINC00261靶向，并减弱了LINC00261对胰腺癌细胞活力，侵袭和凋亡的影响。总之，LINC00261过表达通过降低胰腺癌细胞中miR-23a-3p的表达来抑制细胞活力和侵袭，并增强细胞凋亡，为胰腺癌的治疗提供了新的靶点。LINC00261的加入抑制细胞活力和侵袭并促进细胞凋亡。miR-23a-3p与LINC00261水平呈负相关，miR-23a-3p的高表达表明其生存率较低。miR-23a-3p被LINC00261靶向，并减弱了LINC00261对胰腺癌细胞活力，侵袭和凋亡的影响。总之，LINC00261过表达通过降低胰腺癌细胞中miR-23a-3p的表达来抑制细胞活力和侵袭，并增强细胞凋亡，这是治疗胰腺癌的新靶点。LINC00261的加入抑制细胞活力和侵袭并促进细胞凋亡。miR-23a-3p与LINC00261水平呈负相关，miR-23a-3p的高表达表明其生存率较低。miR-23a-3p被LINC00261靶向，并减弱了LINC00261对胰腺癌细胞活力，侵袭和凋亡的影响。总之，LINC00261过表达通过降低胰腺癌细胞中miR-23a-3p的表达来抑制细胞活力和侵袭，并增强细胞凋亡，这是治疗胰腺癌的新靶点。侵袭和凋亡。总之，LINC00261过表达通过降低胰腺癌细胞中miR-23a-3p的表达来抑制细胞活力和侵袭，并增强细胞凋亡，这是治疗胰腺癌的新靶点。侵袭和凋亡。总之，LINC00261过表达通过降低胰腺癌细胞中miR-23a-3p的表达来抑制细胞活力和侵袭，并增强细胞凋亡，这是治疗胰腺癌的新靶点。