title: A decrease in miR-150 regulates the malignancy of pancreatic cancer by targeting c-Myb and MUC4.
abstract: OBJECTIVE
  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.
authors.affiliation: From the *Department of Pathology, Changhai Hospital, Second Military Medical University; and †Department of Biochemistry and Molecular Biology, Second Military Medical University, Shanghai, China.
authors.forename: Ke
authors.initials: K
authors.lastname: Yang
authors.forename: Miaoxia
authors.initials: M
authors.lastname: He
authors.forename: Zailong
authors.initials: Z
authors.lastname: Cai
authors.forename: Canrong
authors.initials: C
authors.lastname: Ni
authors.forename: Jingjing
authors.initials: J
authors.lastname: Deng
authors.forename: Na
authors.initials: N
authors.lastname: Ta
authors.forename: Jingjing
authors.initials: J
authors.lastname: Xu
authors.forename: Jianming
authors.initials: J
authors.lastname: Zheng
mesh_terms: D000818:Animals; D017209:Apoptosis; D021441:Carcinoma, Pancreatic Ductal / Q000235:genetics / Q000378:metabolism* / Q000401:mortality / Q000473:pathology; D002453:Cell Cycle; D045744:Cell Line, Tumor; D002465:Cell Movement; D049109:Cell Proliferation; D015536:Down-Regulation; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D053208:Kaplan-Meier Estimate; D008297:Male; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D008875:Middle Aged; D055264:Mucin-4 / Q000235:genetics / Q000378:metabolism*; D009361:Neoplasm Invasiveness; D010190:Pancreatic Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000401:mortality / Q000473:pathology; D020598:Proto-Oncogene Proteins c-myb / Q000235:genetics / Q000378:metabolism*; D034622:RNA Interference; D015398:Signal Transduction; D015996:Survival Rate; D013997:Time Factors; D014162:Transfection
chemical_list: D035683:MicroRNAs; D055264:Mucin-4; D020598:Proto-Oncogene Proteins c-myb; C533097:MIR150, human; C524658:MUC4 protein, human