
MicroRNA‐506 is up‐regulated in the development of pancreatic ductal adenocarcinoma and is associated with attenuated disease progression
Author(s) -
Cheng RunFen,
Wang Jian,
Zhang JingYi,
Sun Lin,
Zhao YanRui,
Qiu ZhiQiang,
Sun BaoCun,
Sun Yan
Publication year - 2016
Publication title -
cancer communications
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.119
H-Index - 53
ISSN - 2523-3548
DOI - 10.1186/s40880-016-0128-9
Subject(s) - oncogene , carcinogenesis , microrna , cancer research , ductal cells , biology , pancreatic cancer , metastasis , tumor progression , suppressor , pancreatic ductal adenocarcinoma , pancreas , adenocarcinoma , pathology , medicine , cancer , gene , cell cycle , endocrinology , biochemistry
Background 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. Methods 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. Results 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. Conclusions 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.