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

Erscheinungsjahr:

2024

Erschienen:

2024

Enthalten in:

Zur Gesamtaufnahme - volume:134

Enthalten in:

The International journal of neuroscience - 134(2024), 3 vom: 31. März, Seite 207-213

Sprache:

Englisch

Beteiligte Personen:

Liao, Jiaqi [VerfasserIn]
Xu, Jinxian [VerfasserIn]
Feng, Kaiming [VerfasserIn]
Lai, Wentao [VerfasserIn]
Wen, Xiaohua [VerfasserIn]

Links:

Volltext

Themen:

136601-57-5
CCND1 protein, human
Cyclin D1
GBM
Glioblastoma
Journal Article
MIRN623 microRNA, human
MiR-623
MicroRNAs
RNA, Long Noncoding
RP11-89

Anmerkungen:

Date Completed 04.03.2024

Date Revised 07.03.2024

published: Print-Electronic

Citation Status MEDLINE

doi:

10.1080/00207454.2022.2098734

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM345836715