CircZNF609 and circNFIX as possible regulators of glioblastoma pathogenesis via miR-145-5p/EGFR axis.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
12 06 2024
Historique:
received: 23 02 2024
accepted: 03 06 2024
medline: 13 6 2024
pubmed: 13 6 2024
entrez: 12 6 2024
Statut: epublish

Résumé

Glioblastoma is a rare and deadly malignancy with a low survival rate. Emerging evidence has shown that aberrantly expressed circular RNAs (circRNAs) play a critical role in the initiation and progression of GBM tumorigenesis. The oncogenic function of circZNF609 and circNFIX is involved in several types of cancer, but the role and underlying mechanism of these circRNAs in glioblastoma remain unclear. In this study, we hypothesized that circZNF609 and circNFIX may regulate EGFR through sponging miR-145-5p. Herein, we assessed the expression levels of circZNF609, circNFIX, miR-145-5p, and EGFR using quantitative polymerase chain reaction in glioblastoma patients and normal brain samples. The results showed that circZNF609, circNFIX, and EGFR expression levels were upregulated and miR145-5p was downregulated (p = 0.001, 0.06, 0.002, and 0.0065, respectively), while there was no significant association between clinicopathological features of the patients and the level of these genes expression. We also found a significant inverse correlation between miR145-5p and the expression of cZNF609, cNFIX and EGFR (p = 0.0003, 0.0006, and 0.009, respectively). These findings may open a new window for researchers to better understand the potential pathways involved in GBM pathogenesis. In conclusion, it may provide a new potential pathway for the development of effective drugs for the treatment of GBM patients.

Identifiants

pubmed: 38866807
doi: 10.1038/s41598-024-63827-w
pii: 10.1038/s41598-024-63827-w
doi:

Substances chimiques

MicroRNAs 0
MIRN145 microRNA, human 0
ErbB Receptors EC 2.7.10.1
RNA, Circular 0
EGFR protein, human EC 2.7.10.1
NFI Transcription Factors 0
NFIX protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

13551

Informations de copyright

© 2024. The Author(s).

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Auteurs

Elham Ghadami (E)

Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Ali Gorji (A)

Shefa Neuroscience Research Center, Khatam Al-Anbia Hospital, Tehran, Iran.
Department of Neurosurgery, Westfälische Wilhelms-Universität, Munster, Germany.

Ahmad Pour-Rashidi (A)

Department of Neurosurgery, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran.

Farshid Noorbakhsh (F)

Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Majid Kabuli (M)

Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Masoumeh Razipour (M)

Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Hamid Choobineh (H)

School of Allied Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Mohaddese Maghsudlu (M)

Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Elia Damavandi (E)

Department of Photodynamic, Medical Laser Research Center, Yara Institute, ACECR, Tehran, Iran.
Specialized Medical Genetic Center (SMGC) of ACECR, Tehran, Iran.

Mohsen Ghadami (M)

Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. mghadami@tums.ac.ir.
Cardiac Primary Research Center, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran. mghadami@tums.ac.ir.
Endocrinology and Metabolism Research Institute, Tehran University of Medical Sciences, Tehran, Iran. mghadami@tums.ac.ir.

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