AI Article Synopsis
- Glioma is a deadly brain tumor with stagnant survival rates, necessitating research into its progression mechanisms for potential new treatments.
- The study discovered that TRIM31, a protein that regulates cellular functions, is overexpressed in glioma cells and promotes their growth and invasion by activating the NF-κB signaling pathway.
- Inhibiting NF-κB reversed the effects of TRIM31, suggesting that targeting TRIM31 could be a promising strategy to combat glioma.
Article Abstract
Background: Glioma is the most lethal primary brain tumor, the survival rate still isn't improved in the past decades. It's essential to study the regulatory mechanism of glioma progression, hoping to find new therapy targets or methods. The family of tripartite motif (TRIM) containing proteins are E3 ubiquitination ligases, which play critical role in various tumor progression.
Methods: Cell proliferation and invasion were analyzed by colony formation assay, soft agar growth assay, BrdU incorporation assay and transwell invasion assay. Luciferase reporter analysis was used to analyze NF-κB pathway activity.
Results: We found TRIM31 was upregulated in glioma cells and tissues, its overexpression significantly promoted glioma cell proliferation and invasion, while its knockdown significantly inhibited glioma cell proliferation and invasion. Mechanism analysis found TRIM31 promoted NF-κB pathway activity and increased its targets expression. NF-κB inhibition reversed the phenotype caused by TRIM31, confirming TRIM31 promoted glioma progression through activating NF-κB pathway. Using clinical specimens found TRIM31 expression was positively correlative with NF-κB activity.
Conclusion: This study found TRIM31 promoted glioma proliferation and invasion through activating NF-κB activity.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6441556 | PMC |
| http://dx.doi.org/10.2147/OTT.S183625 | DOI Listing |
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