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Down-regulation of CX43 expression by miR-1 inhibits the proliferation and invasion of glioma cells

BACKGROUND: Connexin (CX) 43 makes glioblastoma resistant to temozolomide, the first-line chemotherapy drug. However, targeting CX43 is very difficult because the mechanisms underlying CX43-mediated resistance remain unclear. CX43 is highly expressed in glioblastoma, which is closely associated with...

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Autores principales: Wang, Gang-Gang, Wang, Yang, Wang, Shi-Long, Zhu, Li-Cang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9745374/
https://www.ncbi.nlm.nih.gov/pubmed/36523292
http://dx.doi.org/10.21037/tcr-22-2318
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author Wang, Gang-Gang
Wang, Yang
Wang, Shi-Long
Zhu, Li-Cang
author_facet Wang, Gang-Gang
Wang, Yang
Wang, Shi-Long
Zhu, Li-Cang
author_sort Wang, Gang-Gang
collection PubMed
description BACKGROUND: Connexin (CX) 43 makes glioblastoma resistant to temozolomide, the first-line chemotherapy drug. However, targeting CX43 is very difficult because the mechanisms underlying CX43-mediated resistance remain unclear. CX43 is highly expressed in glioblastoma, which is closely associated with poor prognosis and chemotherapy resistance. The present study was to analyze the mechanism of microRNA (miR)-1 in regulating the proliferation and invasion of glioma cells. METHODS: The effects of knockdown of miR-1 on the growth of glioma cell lines were observed by establishing blank, miR-1 inhibitor, and miR-1 mimic groups. Cell proliferation was detected using a Cell Counting Kit-8 (CCK-8) assay, cell apoptosis was detected by flow cytometry, and protein expression was detected by western blot. We used the Student’s t-test to assess continuous data between the two groups and the Kruskal-Wallis test was adopted for multiple group comparisons. RESULTS: Compared with the mimics normal control (NC) group, the apoptosis rate of the miR-1-3p mimics group was decreased, while that of the miR-1-3p inhibitor group was increased compared to the inhibitor NC group. In addition, the miR-1-3p mimics model of U251 cells exerted an inhibitory effect on the invasion ability of cells, whereas the miR-1-3p inhibitor model of U251 cells showed an invasion-promoting effect. The dual-luciferase assay showed that miR-1-3p had a targeted relationship with the CX43 gene. CONCLUSIONS: Down-regulation of CX43 expression by miR-1 inhibited the infiltration and growth of glioma cells and further promoted the apoptosis of glioma cells by regulating CX43 expression.
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spelling pubmed-97453742022-12-14 Down-regulation of CX43 expression by miR-1 inhibits the proliferation and invasion of glioma cells Wang, Gang-Gang Wang, Yang Wang, Shi-Long Zhu, Li-Cang Transl Cancer Res Original Article BACKGROUND: Connexin (CX) 43 makes glioblastoma resistant to temozolomide, the first-line chemotherapy drug. However, targeting CX43 is very difficult because the mechanisms underlying CX43-mediated resistance remain unclear. CX43 is highly expressed in glioblastoma, which is closely associated with poor prognosis and chemotherapy resistance. The present study was to analyze the mechanism of microRNA (miR)-1 in regulating the proliferation and invasion of glioma cells. METHODS: The effects of knockdown of miR-1 on the growth of glioma cell lines were observed by establishing blank, miR-1 inhibitor, and miR-1 mimic groups. Cell proliferation was detected using a Cell Counting Kit-8 (CCK-8) assay, cell apoptosis was detected by flow cytometry, and protein expression was detected by western blot. We used the Student’s t-test to assess continuous data between the two groups and the Kruskal-Wallis test was adopted for multiple group comparisons. RESULTS: Compared with the mimics normal control (NC) group, the apoptosis rate of the miR-1-3p mimics group was decreased, while that of the miR-1-3p inhibitor group was increased compared to the inhibitor NC group. In addition, the miR-1-3p mimics model of U251 cells exerted an inhibitory effect on the invasion ability of cells, whereas the miR-1-3p inhibitor model of U251 cells showed an invasion-promoting effect. The dual-luciferase assay showed that miR-1-3p had a targeted relationship with the CX43 gene. CONCLUSIONS: Down-regulation of CX43 expression by miR-1 inhibited the infiltration and growth of glioma cells and further promoted the apoptosis of glioma cells by regulating CX43 expression. AME Publishing Company 2022-11 /pmc/articles/PMC9745374/ /pubmed/36523292 http://dx.doi.org/10.21037/tcr-22-2318 Text en 2022 Translational Cancer Research. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) .
spellingShingle Original Article
Wang, Gang-Gang
Wang, Yang
Wang, Shi-Long
Zhu, Li-Cang
Down-regulation of CX43 expression by miR-1 inhibits the proliferation and invasion of glioma cells
title Down-regulation of CX43 expression by miR-1 inhibits the proliferation and invasion of glioma cells
title_full Down-regulation of CX43 expression by miR-1 inhibits the proliferation and invasion of glioma cells
title_fullStr Down-regulation of CX43 expression by miR-1 inhibits the proliferation and invasion of glioma cells
title_full_unstemmed Down-regulation of CX43 expression by miR-1 inhibits the proliferation and invasion of glioma cells
title_short Down-regulation of CX43 expression by miR-1 inhibits the proliferation and invasion of glioma cells
title_sort down-regulation of cx43 expression by mir-1 inhibits the proliferation and invasion of glioma cells
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9745374/
https://www.ncbi.nlm.nih.gov/pubmed/36523292
http://dx.doi.org/10.21037/tcr-22-2318
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