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Circznf609 and Circnfix As Possible Regulators of Glioblastoma Pathogenesis Via Mir-145-5P/Egfr Axis Publisher Pubmed



Ghadami E1 ; Gorji A2, 3 ; Pourrashidi A4 ; Noorbakhsh F5 ; Kabuli M1 ; Razipour M1 ; Choobineh H6 ; Maghsudlu M1 ; Damavandi E7, 8 ; Ghadami M1, 9, 10
Authors
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Authors Affiliations
  1. 1. Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Shefa Neuroscience Research Center, Khatam Al-Anbia Hospital, Tehran, Iran
  3. 3. Department of Neurosurgery, Westfalische Wilhelms-Universitat, Munster, Germany
  4. 4. Department of Neurosurgery, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran
  5. 5. Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  6. 6. School of Allied Medicine, Tehran University of Medical Sciences, Tehran, Iran
  7. 7. Department of Photodynamic, Medical Laser Research Center, Yara Institute, ACECR, Tehran, Iran
  8. 8. Specialized Medical Genetic Center (SMGC) of ACECR, Tehran, Iran
  9. 9. Cardiac Primary Research Center, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran
  10. 10. Endocrinology and Metabolism Research Institute, Tehran University of Medical Sciences, Tehran, Iran

Source: Scientific Reports Published:2024


Abstract

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. © The Author(s) 2024.