Pancreatic cancer is a malignant disease with poor prognosis. Emerging evidences have showed that miR-597-5p is closely related to tumor development. However, the functional roles of miR-597-5p in pancreatic cancer remain unknown. This study aimed to investigate the expression of miR-597-5p in pancreatic cancer tissues and cells, and explored its regulatory mechanism during pancreatic cancer progression. Pancreatic cancer and adjacent tissues were obtained to detect the expression of miR-597-5p by RT-qPCR. Cell growth, apoptosis, and related protein expression were, respectively, tested by CCK-8 assay, cell formation, wound healing, Transwell assay, flow cytometry, and western blotting. Finally, the pancreatic cancer mice model was constructed. In vitro and in vivo results showed that miR-597-5p expression was down-regulated in pancreatic cancer tissues and cell lines, and increased the overall survival of pancreatic cancer patients. Moreover, miR-597-5p decreased pancreatic cancer cell viability, reduced relative wound width, suppressed colony formation and decreased invasive cell number, as well as reduced the expression of proliferating cell nuclear antigen (PCNA), Ki67, Cyclin D1, N-cad, and Bcl-2. Meanwhile, it increased pancreatic cancer cell apoptosis and the expression of E-cad, cleaved caspase 3, and Bax. The dual-luciferase reporter assay confirmed miR-597-5p could directly target e-twenty six like-1 (ELK1) oncogene. The reduction of cell growth and the induction of cell apoptosis induced by miR-597-5p were reversed by ELK1. In addition, miR-597-5p inhibited the growth of pancreatic cancer in vivo. This study demonstrated that miR-597-5p may be a novel suppressor of pancreatic cancer. It inhibits pancreatic cancer cell growth and promotes apoptosis by the down-regulation of ELK1 in vitro and in vivo.

胰腺癌是一种预后较差的恶性疾病。新出现的证据表明，miR-597-5p与肿瘤发展密切相关。然而，miR-597-5p 在胰腺癌中的功能作用仍然未知。本研究旨在探讨miR-597-5p在胰腺癌组织和细胞中的表达，并探讨其在胰腺癌进展过程中的调控机制。取胰腺癌及癌旁组织，通过RT-qPCR检测miR-597-5p的表达。分别通过CCK-8测定、细胞形成、伤口愈合、Transwell测定、流式细胞术和蛋白质印迹检测细胞生长、凋亡和相关蛋白表达。最后构建胰腺癌小鼠模型。体外和体内结果表明，miR-597-5p 在胰腺癌组织和细胞系中的表达下调，从而提高了胰腺癌患者的总体生存率。此外，miR-597-5p 降低胰腺癌细胞活力、减少相对伤口宽度、抑制集落形成和减少侵袭细胞数量，以及降低增殖细胞核抗原 (PCNA)、Ki67、Cyclin D1、N-cad 的表达, 和 Bcl-2。同时，它增加了胰腺癌细胞的凋亡和 E-cad、cleaved caspase 3 和 Bax 的表达。双荧光素酶报告基因检测证实 miR-597-5p 可以直接靶向 e-26 like-1 (ELK1) 癌基因。由 miR-597-5p 诱导的细胞生长减少和细胞凋亡诱导被 ELK1 逆转。此外，miR-597-5p 在体内抑制胰腺癌的生长。该研究表明，miR-597-5p 可能是一种新型的胰腺癌抑制因子。它通过在体外和体内下调 ELK1 来抑制胰腺癌细胞的生长并促进细胞凋亡。