MiR-623 links lncRNA RP11-89 and cyclin D1 to regulate the proliferation of glioblastoma cells
PURPOSE: The tumorigenesis of bladder cancer has been proven to be related to the increased expression of lncRNA RP11-89, the participation of which in glioblastoma (GBM) is unknown. We predicted that RP11-89 could be targeted by miR-623, which targets cyclin D1. We then analyzed the role of RP11-89 in GBM.
MATERIALS AND METHODS: Samples of both GBM and paired non-tumor tissue were obtained from 58 GBM patients to analyze the expression of RP11-89 and miR-623 through RT-qPCR. The direct binding of miR-623 to RP11-89 was analyzed with RNA-RNA pull down. The role of RP11-89 and miR-623 in regulating each other's expression was analyzed with overexpression assay. The role of RP11-89 and miR-623 in regulating the expression of cyclin D1 and GBM cell proliferation was analyzed by Western blot and BrdU assay, respectively.
RESULTS: RP11-89 was expressed in high amounts in GBM, while miR-623 was expressed in low amounts in GBM. RP11-89 and miR-623 were not closely correlated, while miR-623 directly bound to RP11-89. RP11-89 and miR-623 showed no direct role in each other's expression. RP11-89 suppressed the role of miR-623 in downregulating cyclin D1 and GBM cell proliferation.
CONCLUSIONS: Therefore, miR-623 may link lncRNA RP11-89 and cyclin D1 to regulate the proliferation of GBM cells.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2024 |
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Erschienen: |
2024 |
Enthalten in: |
Zur Gesamtaufnahme - volume:134 |
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Enthalten in: |
The International journal of neuroscience - 134(2024), 3 vom: 31. März, Seite 207-213 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Liao, Jiaqi [VerfasserIn] |
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Links: |
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Themen: |
136601-57-5 |
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Anmerkungen: |
Date Completed 04.03.2024 Date Revised 07.03.2024 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.1080/00207454.2022.2098734 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM345836715 |
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520 | |a PURPOSE: The tumorigenesis of bladder cancer has been proven to be related to the increased expression of lncRNA RP11-89, the participation of which in glioblastoma (GBM) is unknown. We predicted that RP11-89 could be targeted by miR-623, which targets cyclin D1. We then analyzed the role of RP11-89 in GBM | ||
520 | |a MATERIALS AND METHODS: Samples of both GBM and paired non-tumor tissue were obtained from 58 GBM patients to analyze the expression of RP11-89 and miR-623 through RT-qPCR. The direct binding of miR-623 to RP11-89 was analyzed with RNA-RNA pull down. The role of RP11-89 and miR-623 in regulating each other's expression was analyzed with overexpression assay. The role of RP11-89 and miR-623 in regulating the expression of cyclin D1 and GBM cell proliferation was analyzed by Western blot and BrdU assay, respectively | ||
520 | |a RESULTS: RP11-89 was expressed in high amounts in GBM, while miR-623 was expressed in low amounts in GBM. RP11-89 and miR-623 were not closely correlated, while miR-623 directly bound to RP11-89. RP11-89 and miR-623 showed no direct role in each other's expression. RP11-89 suppressed the role of miR-623 in downregulating cyclin D1 and GBM cell proliferation | ||
520 | |a CONCLUSIONS: Therefore, miR-623 may link lncRNA RP11-89 and cyclin D1 to regulate the proliferation of GBM cells | ||
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700 | 1 | |a Wen, Xiaohua |e verfasserin |4 aut | |
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