doi: 10.1186/s40880-016-0128-9
MicroRNA-506 is up-regulated in the development of pancreatic ductal adenocarcinoma and is associated with attenuated disease progression
Run-Fen Cheng, Jian Wang, Jing-Yi Zhang, Lin Sun, Yan-Rui Zhao, Zhi-Qiang Qiu, Bao-Cun Sun and Yan Sun
Department of Pathology, Tianjin Medical University Cancer Institute and Hospital
[Abstract]
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.
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.
Chinese Journal of Cancer 2016, Volume: 35, Issue 12
[ PDF Full-text ]
[ Html full-text / Citation export] (BioMed Central)
[Google Scholar]
Cite this article
Run-Fen Cheng, Jian Wang, Jing-Yi Zhang, Lin Sun, Yan-Rui Zhao, Zhi-Qiang Qiu, Bao-Cun Sun and Yan Sun. MicroRNA-506 is up-regulated in the development of pancreatic ductal adenocarcinoma and is associated with attenuated disease progression. Chin J Cancer. 2016, 35:64. doi:10.1186/s40880-016-0128-9
Export citations
EndNote
[ Html full-text / Citation export] (BioMed Central)
[Google Scholar]
Cite this article
Run-Fen Cheng, Jian Wang, Jing-Yi Zhang, Lin Sun, Yan-Rui Zhao, Zhi-Qiang Qiu, Bao-Cun Sun and Yan Sun. MicroRNA-506 is up-regulated in the development of pancreatic ductal adenocarcinoma and is associated with attenuated disease progression. Chin J Cancer. 2016, 35:64. doi:10.1186/s40880-016-0128-9
Export citations
EndNote
SHARE THIS ARTICLE
Comments:
