Liu Yang-An, Zhang Yue, Zheng Zhi, Li Kai, Wu Xin-Hua, Du Qiu-Guo, Ye Xiao, Wang Lili, Zhu Ling
Department of Hepatobiliary and Pancreatic Surgery, Wuhan Central Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430014, P.R. China.
Department of Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430074, P.R. China.
Oncol Lett. 2018 May;15(5):6745-6751. doi: 10.3892/ol.2018.8109. Epub 2018 Feb 23.
Developments in cancer therapy have greatly improved the survival time for patients with pancreatic ductal adenocarcinoma (PDAC); however, the prognosis of patients with PDAC remains poor. Understanding the expression patterns and functions of microRNAs may provide strategies for the diagnosis and treatment of patients with PDAC. The present study aimed to explore the expression and functions of microRNA-216b (miR-216b) in PDAC. The expression of miR-216b in PDAC tissues and cell lines was quantified with reverse transcription-quantitative polymerase chain reaction. An miR-216b mimic was introduced into PDAC cells to induce the effects of miR-21b overexpression. The effects of miR-216b overexpression on growth, migration and invasion of PDAC cells were evaluated by cell proliferation assay, migration and invasion assays, respectively. The molecular mechanism underlying the suppressive effects of miR-216b on PDAC was also examined; a direct target gene of miR-216b, ρ-associated coiled-coil containing protein kinase 1 (ROCK1), was downregulated by ROCK1 short interfering RNA to investigate the effects on growth, migration and invasion of PDAC cells. The present study revealed that miR-216b was significantly downregulated in PDAC tissues and cell lines. Overexpression of miR-216b inhibited growth, migration and invasion of PDAC cells . ROCK1 was identified as a direct target gene of miR-216b in pancreatic cancer and the downregulation of ROCK1 resembled the effects of miR-216b overexpression in PDAC cells. Taken together, miR-216b acted as a tumor suppressor in PDAC and may represent a novel therapeutic target in PDAC.
癌症治疗的进展极大地延长了胰腺导管腺癌（PDAC）患者的生存时间；然而，PDAC患者的预后仍然很差。了解微小RNA的表达模式和功能可能为PDAC患者的诊断和治疗提供策略。本研究旨在探讨微小RNA-216b（miR-216b）在PDAC中的表达及功能。采用逆转录-定量聚合酶链反应对miR-216b在PDAC组织和细胞系中的表达进行定量。将miR-216b模拟物导入PDAC细胞以诱导miR-21b过表达的效应。分别通过细胞增殖试验、迁移试验和侵袭试验评估miR-216b过表达对PDAC细胞生长、迁移和侵袭的影响。还研究了miR-216b对PDAC抑制作用的分子机制；通过ROCK1短干扰RNA下调miR-216b的直接靶基因——含ρ相关卷曲螺旋的蛋白激酶1（ROCK1），以研究其对PDAC细胞生长、迁移和侵袭的影响。本研究表明，miR-216b在PDAC组织和细胞系中显著下调。miR-216b过表达抑制了PDAC细胞的生长、迁移和侵袭。ROCK1被确定为胰腺癌中miR-216b的直接靶基因，ROCK1的下调类似于miR-216b在PDAC细胞中过表达的效应。综上所述，miR-216b在PDAC中起肿瘤抑制作用，可能是PDAC的一个新的治疗靶点。
