Variances in the Expression Profile of Circadian Clock-Related Genes in Astrocytic Brain Tumors

Author:

Staszkiewicz Rafał123ORCID,Sobański Dawid14ORCID,Pulka Wojciech5,Gładysz Dorian123,Gadzieliński Marcin123,Strojny Damian167ORCID,Grabarek Beniamin Oskar1ORCID

Affiliation:

1. Collegium Medicum, WSB University, 41-300 Dabrowa Gornicza, Poland

2. Department of Neurosurgery, 5th Military Clinical Hospital with the SP ZOZ Polyclinic in Krakow, 30-901 Cracow, Poland

3. Department of Neurosurgery, Faculty of Medicine in Zabrze, Academy of Silesia, 40-555 Katowice, Poland

4. Department of Neurosurgery, Szpital sw. Rafala in Cracow, 30-693 Cracow, Poland

5. Department of Neurosurgery, Neurotraumatology and Spinal Surgery, Regional Hospital in Elblag, 82-300 Elblag, Poland

6. Institute of Health Care, National Academy of Applied Sciences in Przemysl, 37-700 Przemysl, Poland

7. New Medical Techniques Specjalist Hospital of St. Family in Rudna Mała, 36-054 Rudna Mala, Poland

Abstract

This study explores the role of circadian clock genes in the progression of astrocytic tumors, a prevalent type of brain tumor. The aim was to assess the expression patterns of these genes in relation to the tumor grade. Using microarray analysis, qRT-PCR, and methylation-specific PCR, we examined gene expression, DNA methylation patterns, and microRNA interactions in tumor samples from 60 patients. Our results indicate that the expression of key circadian clock genes, such as clock circadian regulator (CLOCK), protein kinase AMP-activated catalytic subunit alpha 1 (PRKAA1), protein kinase AMP-activated catalytic subunit alpha 2 (PRKAA2), protein kinase AMP-activated non-catalytic subunit beta 1 (PRKAB1), protein kinase AMP-activated non-catalytic subunit beta 2 (PRKAB2), period circadian regulator 1 (PER1), period circadian regulator 2 (PER2) and period circadian regulator 3 (PER3), varies significantly with the tumor grade. Notably, increased CLOCK gene expression and protein levels were observed in higher-grade tumors. DNA methylation analysis revealed that the promoter regions of PER1-3 genes were consistently methylated, suggesting a mechanism for their reduced expression. Our findings also underscore the complex regulatory mechanisms involving miRNAs, such as hsa-miR-106-5p, hsa-miR-20b-5p, and hsa-miR-30d-3p, which impact the expression of circadian clock-related genes. This underscores the importance of circadian clock genes in astrocytic tumor progression and highlights their potential as biomarkers and therapeutic targets. Further research is needed to validate these results and explore their clinical implications.

Publisher

MDPI AG

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