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MiR-199 Reverses the Resistance to Gemcitabine in Pancreatic Cancer by Suppressing Stemness through Regulating the Epithelial–Mesenchymal Transition
[Image: see text] Purpose: the present study aims to investigate the function of miR-199 on gemcitabine (GEM)-resistance in pancreatic cancer, as well as the underlying mechanism. Methods: the GEM-resistant SW1990 cell line (SW1990/SZ) was established. The CCK-8 assay was used to detect the cell via...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Chemical Society
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8637594/ https://www.ncbi.nlm.nih.gov/pubmed/34869970 http://dx.doi.org/10.1021/acsomega.1c02945 |
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author | Wei, Weitian Wang, Liang Xu, Liwei Liang, Jinxiao Teng, Lisong |
author_facet | Wei, Weitian Wang, Liang Xu, Liwei Liang, Jinxiao Teng, Lisong |
author_sort | Wei, Weitian |
collection | PubMed |
description | [Image: see text] Purpose: the present study aims to investigate the function of miR-199 on gemcitabine (GEM)-resistance in pancreatic cancer, as well as the underlying mechanism. Methods: the GEM-resistant SW1990 cell line (SW1990/SZ) was established. The CCK-8 assay was used to detect the cell viability. The self-renewal of SW1990/SZ cells was evaluated by sphere formation and the colony formation assay. The apoptosis was detected by flow cytometry and the migration ability was measured by the transwell assay. The dual-luciferase gene reporter assay was utilized to confirm the binding between miR-199 and Snail. The expression level of CD44, ALDH1, Nanog, E-cadherin, Vimentin, β-catenin, and Snail was determined by the Western blotting assay. Results: the cell sphere formation rate, number of spheres, and expression level of CD44, ALDH1, and Nanog in GEM-treated SW1990/SZ cells were significantly suppressed by miR-199, accompanied by declined proliferation ability, an increased apoptotic rate, inhibited migration ability, and suppressed EMT progression. The binding site between miR-199 and 3′-UTR of Snail was predicted and confirmed. The inhibitory effect of miR-199 on self-renewal of SW1990/GZ cells and the faciliating property of miR-199 on the inhibitory effect of GEM against the proliferation ability, migration ability, and EMT progression were abolished by overexpressing Snail. Conclusion: MiR-199 reversed the resistance to GEM in pancreatic cancer by suppressing stemness through regulating the EMT. |
format | Online Article Text |
id | pubmed-8637594 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | American Chemical Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-86375942021-12-03 MiR-199 Reverses the Resistance to Gemcitabine in Pancreatic Cancer by Suppressing Stemness through Regulating the Epithelial–Mesenchymal Transition Wei, Weitian Wang, Liang Xu, Liwei Liang, Jinxiao Teng, Lisong ACS Omega [Image: see text] Purpose: the present study aims to investigate the function of miR-199 on gemcitabine (GEM)-resistance in pancreatic cancer, as well as the underlying mechanism. Methods: the GEM-resistant SW1990 cell line (SW1990/SZ) was established. The CCK-8 assay was used to detect the cell viability. The self-renewal of SW1990/SZ cells was evaluated by sphere formation and the colony formation assay. The apoptosis was detected by flow cytometry and the migration ability was measured by the transwell assay. The dual-luciferase gene reporter assay was utilized to confirm the binding between miR-199 and Snail. The expression level of CD44, ALDH1, Nanog, E-cadherin, Vimentin, β-catenin, and Snail was determined by the Western blotting assay. Results: the cell sphere formation rate, number of spheres, and expression level of CD44, ALDH1, and Nanog in GEM-treated SW1990/SZ cells were significantly suppressed by miR-199, accompanied by declined proliferation ability, an increased apoptotic rate, inhibited migration ability, and suppressed EMT progression. The binding site between miR-199 and 3′-UTR of Snail was predicted and confirmed. The inhibitory effect of miR-199 on self-renewal of SW1990/GZ cells and the faciliating property of miR-199 on the inhibitory effect of GEM against the proliferation ability, migration ability, and EMT progression were abolished by overexpressing Snail. Conclusion: MiR-199 reversed the resistance to GEM in pancreatic cancer by suppressing stemness through regulating the EMT. American Chemical Society 2021-11-17 /pmc/articles/PMC8637594/ /pubmed/34869970 http://dx.doi.org/10.1021/acsomega.1c02945 Text en © 2021 The Authors. Published by American Chemical Society https://creativecommons.org/licenses/by-nc-nd/4.0/Permits non-commercial access and re-use, provided that author attribution and integrity are maintained; but does not permit creation of adaptations or other derivative works (https://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Wei, Weitian Wang, Liang Xu, Liwei Liang, Jinxiao Teng, Lisong MiR-199 Reverses the Resistance to Gemcitabine in Pancreatic Cancer by Suppressing Stemness through Regulating the Epithelial–Mesenchymal Transition |
title | MiR-199 Reverses the Resistance to Gemcitabine in
Pancreatic Cancer by Suppressing Stemness through Regulating the Epithelial–Mesenchymal
Transition |
title_full | MiR-199 Reverses the Resistance to Gemcitabine in
Pancreatic Cancer by Suppressing Stemness through Regulating the Epithelial–Mesenchymal
Transition |
title_fullStr | MiR-199 Reverses the Resistance to Gemcitabine in
Pancreatic Cancer by Suppressing Stemness through Regulating the Epithelial–Mesenchymal
Transition |
title_full_unstemmed | MiR-199 Reverses the Resistance to Gemcitabine in
Pancreatic Cancer by Suppressing Stemness through Regulating the Epithelial–Mesenchymal
Transition |
title_short | MiR-199 Reverses the Resistance to Gemcitabine in
Pancreatic Cancer by Suppressing Stemness through Regulating the Epithelial–Mesenchymal
Transition |
title_sort | mir-199 reverses the resistance to gemcitabine in
pancreatic cancer by suppressing stemness through regulating the epithelial–mesenchymal
transition |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8637594/ https://www.ncbi.nlm.nih.gov/pubmed/34869970 http://dx.doi.org/10.1021/acsomega.1c02945 |
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