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Upregulation of microRNA-1270 suppressed human glioblastoma cancer cell proliferation migration and tumorigenesis by acting through WT1
BACKGROUND: Glioblastoma multiforme (GBM) is one of the most aggressive brain tumors among human beings. In this study, we explored the functions of human microRNA-1270 (hsa-miR-1270) on GBM cancer cell proliferation, migration, and tumorigenesis. MATERIALS AND METHODS: In GBM cell lines and clinica...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Dove Medical Press
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6592694/ https://www.ncbi.nlm.nih.gov/pubmed/31417281 http://dx.doi.org/10.2147/OTT.S192521 |
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author | Wei, Lai Li, Pan Zhao, Chunjing Wang, Na Wei, Na |
author_facet | Wei, Lai Li, Pan Zhao, Chunjing Wang, Na Wei, Na |
author_sort | Wei, Lai |
collection | PubMed |
description | BACKGROUND: Glioblastoma multiforme (GBM) is one of the most aggressive brain tumors among human beings. In this study, we explored the functions of human microRNA-1270 (hsa-miR-1270) on GBM cancer cell proliferation, migration, and tumorigenesis. MATERIALS AND METHODS: In GBM cell lines and clinical tissues, hsa-miR-1270 expression was probed by quantitative real-time PCR (qRT-PCR). In LN-18 and A172 cells, hsa-miR-1270 was upregulated by lentiviral transduction. The effects of hsa-miR-1270 upregulation on GBM in vitro and in vivo functions were probed by proliferation, migration, and xenograft assays, respectively. The correlation between hsa-miR-1270 and Wilms’ tumor gene (WT1) was probed by dual-luciferase activity assay, qRT-PCR, and Western blot. WT1 was then secondarily over-expressed in hsa-miR-1270-upregulated LN-18 and A172 cells, to explore its mechanisms in GBM’s association with hsa-miR-1270. RESULTS: Hsa-miR-1270 was significantly downregulated in both GBM cell lines and clinical tumors. Upregulating hsa-miR-1270 considerably suppressed GBM cell proliferation and migration in vitro and xenograft in vivo. WT1 was inversely correlated with hsa-miR-1270 in GBM. WT1 overexpression in hsa-miR-1270-upregulated GBM cells reversed the anticancer functions of hsa-miR-1270 on cancer proliferation and migration. CONCLUSION: Hsa-miR-1270 upregulation may have suppressing effects on GBM cancer cells, likely by functionally acting through WT1. |
format | Online Article Text |
id | pubmed-6592694 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-65926942019-08-15 Upregulation of microRNA-1270 suppressed human glioblastoma cancer cell proliferation migration and tumorigenesis by acting through WT1 Wei, Lai Li, Pan Zhao, Chunjing Wang, Na Wei, Na Onco Targets Ther Original Research BACKGROUND: Glioblastoma multiforme (GBM) is one of the most aggressive brain tumors among human beings. In this study, we explored the functions of human microRNA-1270 (hsa-miR-1270) on GBM cancer cell proliferation, migration, and tumorigenesis. MATERIALS AND METHODS: In GBM cell lines and clinical tissues, hsa-miR-1270 expression was probed by quantitative real-time PCR (qRT-PCR). In LN-18 and A172 cells, hsa-miR-1270 was upregulated by lentiviral transduction. The effects of hsa-miR-1270 upregulation on GBM in vitro and in vivo functions were probed by proliferation, migration, and xenograft assays, respectively. The correlation between hsa-miR-1270 and Wilms’ tumor gene (WT1) was probed by dual-luciferase activity assay, qRT-PCR, and Western blot. WT1 was then secondarily over-expressed in hsa-miR-1270-upregulated LN-18 and A172 cells, to explore its mechanisms in GBM’s association with hsa-miR-1270. RESULTS: Hsa-miR-1270 was significantly downregulated in both GBM cell lines and clinical tumors. Upregulating hsa-miR-1270 considerably suppressed GBM cell proliferation and migration in vitro and xenograft in vivo. WT1 was inversely correlated with hsa-miR-1270 in GBM. WT1 overexpression in hsa-miR-1270-upregulated GBM cells reversed the anticancer functions of hsa-miR-1270 on cancer proliferation and migration. CONCLUSION: Hsa-miR-1270 upregulation may have suppressing effects on GBM cancer cells, likely by functionally acting through WT1. Dove Medical Press 2019-06-20 /pmc/articles/PMC6592694/ /pubmed/31417281 http://dx.doi.org/10.2147/OTT.S192521 Text en © 2019 Wei et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. |
spellingShingle | Original Research Wei, Lai Li, Pan Zhao, Chunjing Wang, Na Wei, Na Upregulation of microRNA-1270 suppressed human glioblastoma cancer cell proliferation migration and tumorigenesis by acting through WT1 |
title | Upregulation of microRNA-1270 suppressed human glioblastoma cancer cell proliferation migration and tumorigenesis by acting through WT1 |
title_full | Upregulation of microRNA-1270 suppressed human glioblastoma cancer cell proliferation migration and tumorigenesis by acting through WT1 |
title_fullStr | Upregulation of microRNA-1270 suppressed human glioblastoma cancer cell proliferation migration and tumorigenesis by acting through WT1 |
title_full_unstemmed | Upregulation of microRNA-1270 suppressed human glioblastoma cancer cell proliferation migration and tumorigenesis by acting through WT1 |
title_short | Upregulation of microRNA-1270 suppressed human glioblastoma cancer cell proliferation migration and tumorigenesis by acting through WT1 |
title_sort | upregulation of microrna-1270 suppressed human glioblastoma cancer cell proliferation migration and tumorigenesis by acting through wt1 |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6592694/ https://www.ncbi.nlm.nih.gov/pubmed/31417281 http://dx.doi.org/10.2147/OTT.S192521 |
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