| Literature DB >> 29196101 |
Zhengliang Zhang1, Xiangming Che2, Ni Yang1, Zhenghai Bai1, Yuan Wu1, Li Zhao1, Honghong Pei3.
Abstract
The exact mechanisms of metastasis for pancreatic cancer remain to be uncovered. This study aimed to elucidate the potential functional mechanism of miR-135b-5p in migration, invasion and epithelial-to-mesenchymal transition (EMT) of pancreatic cancer cells. By real-time PCR and analysis of GEO database, we determined the up-regulated expression of miR-135b-5p in pancreatic cancer tissues and cell lines. Clinically, highly expressed miR-135b-5p was closely related to advanced TNM stage, more lymph node metastasis, more distant metastasis and worse overall survival (OS) and disease-free survival (DFS). Functionally, Transwell assays indicated that miR-135b-5p was a promoter for migration and invasion of pancreatic cancer cells. Additionally, immunohistochemistry staining and Western blot showed that highly expressed miR-135b-5p accelerated EMT process of pancreatic cancer cells. Furthermore, a series of experiments and rescue experiments revealed that Nuclear Receptor Subfamily 3 Group C Member 2 (NR3C2) was the target of miR-135b-5p in pancreatic cancer cells, mediating the promotion effects of miR-135b-5p on the tumor cells migration, invasion and EMT. In conclusion, miR-135b-5p, maybe a novel therapeutic target for pancreatic cancer, promoted migration, invasion and EMT of pancreatic cancer cells by targeting NR3C2.Entities:
Keywords: Epithelial-to-mesenchymal transition; Invasion; Migration; Pancreatic cancer; miR-135b-5p
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Year: 2017 PMID: 29196101 DOI: 10.1016/j.biopha.2017.11.074
Source DB: PubMed Journal: Biomed Pharmacother ISSN: 0753-3322 Impact factor: 6.529