title: MicroRNA-506 is up-regulated in the development of pancreatic ductal adenocarcinoma and is associated with attenuated disease progression.
abstract: MicroRNA-506 (miR-506) has been reported to function in several tumors as a tumor suppressor gene or oncogene. However, the expression and role of miR-506 in pancreatic ductal adenocarcinoma (PDAC) remains unclear. In this study, we aimed to evaluate the phenotype of miR-506 in PDAC.
  
  
  
  Using miRNA in situ hybridization, we examined the expression of miR-506 in 113 PDACs and 87 paired normal pancreatic tissues. We evaluated miR-506 expression in PDAC cells, normal pancreatic ducts, and acinus/islands, and we analyzed the associations between miR-506 expression and the clinicopathologic characteristics of PDAC patients.
  
  
  
  miR-506 expression was higher in PDAC than in matched normal pancreatic ductal cells (P < 0.001). On the other hand, the combined group of well and moderately differentiated PDACs showed higher levels of miR-506 than the poorly differentiated ones (P = 0.023). Moreover, miR-506 expression was negatively associated with pathologic T category (P = 0.004) and lymph node metastasis (P = 0.033), suggesting that miR-506 might inhibit the progression of PDAC.
  
  
  
  Our results suggest that miR-506 either plays a role as an oncogene in the tumorigenesis and a tumor suppressor in the progression or serves as a house-keeping, tumor-suppressing miRNA, whose expression can be activated by oncogenic signals in early development to hinder the progression of PDAC.
authors.affiliation: Department of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, P. R. China.
authors.forename: Run-Fen
authors.initials: RF
authors.lastname: Cheng
authors.affiliation: Department of Pancreatic Oncology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, P. R. China.
authors.forename: Jian
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, P. R. China.
authors.forename: Jing-Yi
authors.initials: JY
authors.lastname: Zhang
authors.affiliation: Department of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, P. R. China.
authors.forename: Lin
authors.initials: L
authors.lastname: Sun
authors.affiliation: Department of Epidemiology and Biostatistics, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, P. R. China.
authors.forename: Yan-Rui
authors.initials: YR
authors.lastname: Zhao
authors.affiliation: Department of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, P. R. China.
authors.forename: Zhi-Qiang
authors.initials: ZQ
authors.lastname: Qiu
authors.affiliation: Department of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, P. R. China.|Department of Pathology, Tianjin Medical University, Tianjin, 300070, P. R. China.
authors.forename: Bao-Cun
authors.initials: BC
authors.lastname: Sun
authors.affiliation: Department of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, P. R. China. sunyan@tjmuch.com.
authors.forename: Yan
authors.initials: Y
authors.lastname: Sun
mesh_terms: D000328:Adult; D000368:Aged; D021441:Carcinoma, Pancreatic Ductal / Q000235:genetics* / Q000473:pathology*; D016022:Case-Control Studies; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008297:Male; D035683:MicroRNAs / Q000235:genetics*; D008875:Middle Aged; D010190:Pancreatic Neoplasms / Q000235:genetics* / Q000473:pathology*; D015854:Up-Regulation
chemical_list: C561508:MIRN506 microRNA, human; D035683:MicroRNAs
keywords: Development; Pancreatic ductal adenocarcinoma; Progression; Tumor suppressor; miR-506