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

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...

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Autores principales: Xue, Liang, Shen, Yan, Zhai, Zhenglong, Zheng, Shusen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7169848/
https://www.ncbi.nlm.nih.gov/pubmed/32236568
http://dx.doi.org/10.3892/ijmm.2020.4561
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author Xue, Liang
Shen, Yan
Zhai, Zhenglong
Zheng, Shusen
author_facet Xue, Liang
Shen, Yan
Zhai, Zhenglong
Zheng, Shusen
author_sort Xue, Liang
collection PubMed
description 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.
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spelling pubmed-71698482020-04-24 miR-539 suppresses the proliferation, migration, invasion and epithelial mesenchymal transition of pancreatic cancer cells through targeting SP1 Xue, Liang Shen, Yan Zhai, Zhenglong Zheng, Shusen Int J Mol Med Articles 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. D.A. Spandidos 2020-06 2020-04-01 /pmc/articles/PMC7169848/ /pubmed/32236568 http://dx.doi.org/10.3892/ijmm.2020.4561 Text en Copyright: © Xue et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Xue, Liang
Shen, Yan
Zhai, Zhenglong
Zheng, Shusen
miR-539 suppresses the proliferation, migration, invasion and epithelial mesenchymal transition of pancreatic cancer cells through targeting SP1
title miR-539 suppresses the proliferation, migration, invasion and epithelial mesenchymal transition of pancreatic cancer cells through targeting SP1
title_full miR-539 suppresses the proliferation, migration, invasion and epithelial mesenchymal transition of pancreatic cancer cells through targeting SP1
title_fullStr miR-539 suppresses the proliferation, migration, invasion and epithelial mesenchymal transition of pancreatic cancer cells through targeting SP1
title_full_unstemmed miR-539 suppresses the proliferation, migration, invasion and epithelial mesenchymal transition of pancreatic cancer cells through targeting SP1
title_short miR-539 suppresses the proliferation, migration, invasion and epithelial mesenchymal transition of pancreatic cancer cells through targeting SP1
title_sort mir-539 suppresses the proliferation, migration, invasion and epithelial mesenchymal transition of pancreatic cancer cells through targeting sp1
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7169848/
https://www.ncbi.nlm.nih.gov/pubmed/32236568
http://dx.doi.org/10.3892/ijmm.2020.4561
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