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Marsdenia tenacissima extract prevents the malignant progression of glioma through upregulating lncRNA MEG3 and SFRP1‐dependent inhibition of Wnt/β‐catenin pathway
BACKGROUND/AIM: Recent studies have highlighted the tumor‐suppressive effect of Marsdenia tenacissima extract (MTE) on human cancers. This research unveils the potential impact of MTE on glioma and ascertains the relevant molecular mechanisms. METHODS: Glioma cells were treated with MTE, with normal...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10068475/ https://www.ncbi.nlm.nih.gov/pubmed/36756719 http://dx.doi.org/10.1111/cns.14100 |
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author | Chen, Lei Gong, Xin Huang, Mengyi |
author_facet | Chen, Lei Gong, Xin Huang, Mengyi |
author_sort | Chen, Lei |
collection | PubMed |
description | BACKGROUND/AIM: Recent studies have highlighted the tumor‐suppressive effect of Marsdenia tenacissima extract (MTE) on human cancers. This research unveils the potential impact of MTE on glioma and ascertains the relevant molecular mechanisms. METHODS: Glioma cells were treated with MTE, with normal human astrocytes (NHAs) as controls. A battery of function experiments, including the CCK‐8 viability test, colony formation assay, scratch migration assay, and Transwell invasion assay, was executed to address the responses of glioma cells to MTE treatment and gain or loss of function of lncMEG3, miR‐542‐3p, and SFRP1. FISH, RIP, and dual‐luciferase reporter assays were adopted for assessing gene interactions. U251‐GFP‐Luc cells were delivered into nude mice through intracranial injection to develop an orthotopic glioma model for in vivo validation. RESULTS: 200 mg/mL MTE could suppress the proliferating, migrating, and invading properties of glioma cells but not affect those of NHAs. MTE treatment enhanced the expression of lncMEG3, which competes with SFRP1 for binding miR‐542‐3p. SFRP1 could inactivate the Wnt/β‐catenin pathway. Animal experimentation substantiated the antitumor activity and mechanism of MTE in nude mice. CONCLUSIONS: MTE suppresses glioma via the lncMEG3/miR‐542‐3p/SFRP1/Wnt/β‐catenin axis. These findings contribute to a theoretical basis for the use of MTE for glioma patients. |
format | Online Article Text |
id | pubmed-10068475 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-100684752023-04-04 Marsdenia tenacissima extract prevents the malignant progression of glioma through upregulating lncRNA MEG3 and SFRP1‐dependent inhibition of Wnt/β‐catenin pathway Chen, Lei Gong, Xin Huang, Mengyi CNS Neurosci Ther Original Articles BACKGROUND/AIM: Recent studies have highlighted the tumor‐suppressive effect of Marsdenia tenacissima extract (MTE) on human cancers. This research unveils the potential impact of MTE on glioma and ascertains the relevant molecular mechanisms. METHODS: Glioma cells were treated with MTE, with normal human astrocytes (NHAs) as controls. A battery of function experiments, including the CCK‐8 viability test, colony formation assay, scratch migration assay, and Transwell invasion assay, was executed to address the responses of glioma cells to MTE treatment and gain or loss of function of lncMEG3, miR‐542‐3p, and SFRP1. FISH, RIP, and dual‐luciferase reporter assays were adopted for assessing gene interactions. U251‐GFP‐Luc cells were delivered into nude mice through intracranial injection to develop an orthotopic glioma model for in vivo validation. RESULTS: 200 mg/mL MTE could suppress the proliferating, migrating, and invading properties of glioma cells but not affect those of NHAs. MTE treatment enhanced the expression of lncMEG3, which competes with SFRP1 for binding miR‐542‐3p. SFRP1 could inactivate the Wnt/β‐catenin pathway. Animal experimentation substantiated the antitumor activity and mechanism of MTE in nude mice. CONCLUSIONS: MTE suppresses glioma via the lncMEG3/miR‐542‐3p/SFRP1/Wnt/β‐catenin axis. These findings contribute to a theoretical basis for the use of MTE for glioma patients. John Wiley and Sons Inc. 2023-02-08 /pmc/articles/PMC10068475/ /pubmed/36756719 http://dx.doi.org/10.1111/cns.14100 Text en © 2023 The Authors. CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Chen, Lei Gong, Xin Huang, Mengyi Marsdenia tenacissima extract prevents the malignant progression of glioma through upregulating lncRNA MEG3 and SFRP1‐dependent inhibition of Wnt/β‐catenin pathway |
title | Marsdenia tenacissima extract prevents the malignant progression of glioma through upregulating lncRNA MEG3 and SFRP1‐dependent inhibition of Wnt/β‐catenin pathway |
title_full | Marsdenia tenacissima extract prevents the malignant progression of glioma through upregulating lncRNA MEG3 and SFRP1‐dependent inhibition of Wnt/β‐catenin pathway |
title_fullStr | Marsdenia tenacissima extract prevents the malignant progression of glioma through upregulating lncRNA MEG3 and SFRP1‐dependent inhibition of Wnt/β‐catenin pathway |
title_full_unstemmed | Marsdenia tenacissima extract prevents the malignant progression of glioma through upregulating lncRNA MEG3 and SFRP1‐dependent inhibition of Wnt/β‐catenin pathway |
title_short | Marsdenia tenacissima extract prevents the malignant progression of glioma through upregulating lncRNA MEG3 and SFRP1‐dependent inhibition of Wnt/β‐catenin pathway |
title_sort | marsdenia tenacissima extract prevents the malignant progression of glioma through upregulating lncrna meg3 and sfrp1‐dependent inhibition of wnt/β‐catenin pathway |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10068475/ https://www.ncbi.nlm.nih.gov/pubmed/36756719 http://dx.doi.org/10.1111/cns.14100 |
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