miR-539 suppresses the proliferation, migration, invasion and epithelial mesenchymal transition of pancreatic cancer cells through targeting SP1

被引:11
作者
Xue, Liang [1 ]
Shen, Yan [1 ]
Zhai, Zhenglong [1 ]
Zheng, Shusen [1 ]
机构
[1] Zhejiang Univ, Affiliated Hosp 1, Dept Hepatobiliary & Pancreat Surg, 79 Qingchun Rd, Hangzhou 310003, Zhejiang, Peoples R China
关键词
miR-539; target gene; pancreatic cancer; development; progression; TRANSCRIPTION FACTOR; TUMOR-SUPPRESSOR; BREAST-CANCER; LUNG-CANCER; PROGRESSION; GROWTH; EXPRESSION; PROMOTES; MANAGEMENT; ADENOCARCINOMA;
D O I
10.3892/ijmm.2020.4561
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
MicroRNA (miR)-539 has inhibitory effects on certain types of cancer, but its role in pancreatic cancer (PCa) remains unclear. The present study investigated the effects of miR-539 on PCa, and aimed to determine possible therapeutic targets for the treatment of PCa. The expression of miR-539 in PCa tissues, paired normal adjacent tissues and PCa cell lines (CAPAN-2, BxPC3, CFPAC1, SW1990 and PANC1), and human non-cancerous pancreatic cells (hTRET-HPNE) was determined and compared. The effects of upregulation and downregulation of miR-539 on proliferation, apoptosis, cell cycle, invasion, migration and epithelial-mesenchymal transition (EMT) of PCa cells were investigated. Additionally, the target gene of miR-539 was predicted and its effects on PCa cells were further investigated. The results revealed low expression of miR-539 in PCa tissues and cell lines. Additionally, increasing miR-539 expression inhibited the proliferation, migration, invasion and EMT of PCa cells and induced apoptosis by blocking G1 phase of the cell cycle, while reducing miR-539 expression had the opposite results. Furthermore, specificity protein 1 (SP1) was found to be the target gene of miR-539. SP1 promoted the proliferation, migration, invasion and EMT transformation of PCa cells, but these effects were reversed by high expression of miR-539. Additionally, miR-539 suppressed the proliferation, metastasis, invasion and EMT transformation of PCa cells through targeting SP1. Therefore, miR-539 overexpression may contribute toward development of novel therapeutic strategies for PCa in the future.
引用
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页码:1771 / 1782
页数:12
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