A Decrease in miR-150 Regulates the Malignancy of Pancreatic Cancer by Targeting c-Myb and MUC4. Issue 3 (April 2015)

• Record Type: Journal Article
• Authors: Yang, Ke; He, Miaoxia; Cai, Zailong; Ni, Canrong; Deng, Jingjing; Ta, Na; Xu, Jingjing; Zheng, Jianming
• Is Part Of: Pancreas. Volume 44:Issue 3(2015)
• Publication Date: 2015-04
• Subjects: miR-150 -- pancreatic cancer -- tumor-suppressor miRNA -- c-Myb and MUC4; Pancreas -- Diseases -- Periodicals; Pancreas -- Periodicals; Neuroendocrine tumors -- Periodicals; 616.37005
• DOI: 10.1097/MPA.0000000000000283
• Languages: English
• ISSNs: 0885-3177

Abstract

Abstract : Objectives: Pancreatic cancer is an aggressive cancer with high mortality. Conventional treatments have little impact on its progression. Limited research investigating the role of oncogene miR-150 specifically in pancreatic cancer has been published. The purpose of this study was to determine the tumorigenesis of miR-150 in pancreatic cancer. Methods: One hundred six pancreatic ductal adenocarcinomas were analyzed together with their adjacent benign pancreatic tissues. The associations of miR-150, c-Myb, and MUC4 expression with survival rates were determined. Functional studies on miR-150 in pancreatic cancer were used to assess its effect on proliferation and malignancy in several pancreatic cell lines. Results: miR-150 expression was significantly down-regulated in pancreatic ductal adenocarcinoma tissues compared with adjacent benign pancreatic tissues. Patients with low miR-150 expression had significantly higher mortality rates than those with high miR-150 expression. The in vitro and in vivo assays of pancreatic cancer cells showed that miR-150 overexpression leads to reduced cell growth, clonogenicity, migration, invasion, modular cell cycles, and induced apoptosis. Moreover, miR-150 expression was inversely correlated with c-Myb and MUC4 activities in pancreatic tissue, cell lines, and nude mouse model. Conclusions: miR-150 is an important suppressor of pancreatic ductal carcinoma and acts as a regulator of c-Myb and MUC4 in aggressive progress. Abstract : Supplemental digital content is available in the text.