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A Decrease in miR-150 Regulates the Malignancy of Pancreatic Cancer by Targeting c-Myb and MUC4

Yang, Ke MS*; He, Miaoxia MD, PhD*; Cai, Zailong PhD; Ni, Canrong BS*; Deng, Jingjing MS*; Ta, Na MS*; Xu, Jingjing BS*; Zheng, Jianming MD, PhD*

doi: 10.1097/MPA.0000000000000283
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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.

Supplemental digital content is available in the text.

From the *Department of Pathology, Changhai Hospital, Second Military Medical University; and †Department of Biochemistry and Molecular Biology, Second Military Medical University, Shanghai, China.

Received for publication November 20, 2013; accepted August 18, 2014.

Reprints: Jianming Zheng, MD, PhD, Department of Pathology, Changhai Hospital, Second Military Medical University, 168 Changhai Rd, Shanghai, 200433 China (e-mail: jmzheng1962@163.com); and Zailong Cai, PhD, Department of Biochemistry and Molecular Biology, Second Military Medical University, 800 Xiangyin Rd, Shanghai, 200433 China (e-mail: czl8003@hotmail.com).

This study was supported by the National Natural Science Foundation of China (project no. 81172077) and the Shanghai Biobank Network of Common Human Tumor Tissue Fund (project no. 12DZ2295102).

The authors declare no conflict of interest.

Author Contributions: Conceived and designed the experiments: J.Z. and Z.C. Performed the experiments: K.Y. and M.H. Analyzed the data: M.H. and K.Y. Contributed the reagents/materials/analysis tools: K.Y. and J.D. Wrote the article: M.H. and J.Z.

Ke Yang and Miaoxia He worked equally in this study.

Supplemental digital contents are available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s Web site (www.pancreasjournal.com).

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