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Impact of endogenous viral elements on glioma clinical phenotypes by inducing OCT4 in the host
Shirong Li1, Shuai He1, Haoyu Xue2
1Department of Neurosurgery and Laboratory of Animal Tumor Models, Cancer Center and Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Introduction:
Endogenous viral elements (EVEs) are viral sequences integrated within the host genome that can influence gene regulation and tumor development. While EVEs have been implicated in cancer, their role in regulating key transcription factors in glioblastoma (GBM) remains underexplored. This study investigates the relationship between EVEs and the activation of OCT4, a critical transcription factor in GBM progression.
Methods:
We utilized CancerHERVdb and HervD Atlas databases to identify potential interactions between EVEs and key genes involved in GBM. Data from 273 GBM patient samples in the TCGA database were analyzed to examine the correlation between OCT4 expression and mutations in glioma-related genes. Furthermore, glioblastoma stem cells (GSCs) were assessed for the expression levels of OCT4 and SOX2, and Pearson correlation analysis was performed.
Results:
Our analysis revealed that OCT4 is a pivotal gene activated by EVEs in GBM. OCT4 expression was significantly correlated with mutations in key glioma-associated genes. Higher OCT4 levels were associated with poorer patient prognosis, higher tumor grades, and older age. Additionally, GSCs exhibited elevated expression of both OCT4 and SOX2, with a positive correlation observed between these two genes in GBM patients.
Discussion:
This study highlights the potential role of EVEs in driving GBM progression through the activation of OCT4. The findings emphasize the importance of OCT4 in GBM malignancy and suggest that targeting EVE-mediated pathways may provide new therapeutic approaches for GBM treatment.
Insights
Endogenous viral elements (EVEs) activate OCT4, a key gene in glioblastoma (GBM) progression. This EVE-OCT4 link impacts GBM malignancy and patient prognosis, suggesting new therapeutic targets.
Area of Science:
- Oncology
- Molecular Biology
- Genomics
Background:
- Endogenous viral elements (EVEs) are integrated viral sequences influencing host gene regulation and cancer development.
- The role of EVEs in regulating critical transcription factors in glioblastoma (GBM) is not well understood.
- OCT4 is a key transcription factor implicated in GBM progression.
Purpose of the Study:
- To investigate the relationship between EVEs and OCT4 activation in GBM.
- To explore the correlation between OCT4 expression, glioma-associated gene mutations, and patient outcomes.
- To assess OCT4 and SOX2 expression in glioblastoma stem cells (GSCs).
Main Methods:
- Utilized CancerHERVdb and HervD Atlas databases for EVE-gene interaction analysis.
- Analyzed TCGA data from 273 GBM patients for OCT4 expression and gene mutations.
- Assessed OCT4 and SOX2 expression in GSCs and performed Pearson correlation analysis.
Main Results:
- OCT4 is a pivotal gene activated by EVEs in GBM.
- OCT4 expression significantly correlated with mutations in glioma-associated genes.
- Elevated OCT4 levels were linked to poorer prognosis, higher tumor grade, and older age.
- GSCs showed increased OCT4 and SOX2 expression, with a positive correlation between them.
Conclusions:
- EVEs may drive GBM progression via OCT4 activation.
- OCT4 plays a significant role in GBM malignancy.
- Targeting EVE-mediated pathways presents a potential therapeutic strategy for GBM.
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