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Updated: Mar 21, 2026
The Clinical Application of Tumor Treating Fields Therapy in Glioblastoma
Published on: April 16, 2019
TUSC3 suppresses glioblastoma development by inhibiting Akt signaling
Zhenfeng Jiang1, Mian Guo2, Xiangtong Zhang1
1Department of Neurosurgery, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Harbin, Heilongjiang Province, 150001, China.
Abstract:
Glioblastoma multiform is one of the most common and most aggressive brain tumors in humans. The molecular and cellular mechanisms responsible for the onset and progression of GBM are elusive and controversial. The function of tumor suppressor candidate 3 (TUSC3) has not been previously characterized in GBM. TUSC3 was originally identified as part of an enzyme complex involved in N-glycosylation of proteins, but was recently implicated as a potential tumor suppressor gene in a variety of cancer types. In this study, we demonstrated that the expression levels of TUSC3 were downregulated in both GBM tissues and cells, and also found that overexpression of TUSC3 inhibits GBM cell proliferation and invasion. In addition, the effects of increased levels of methylation on the TUSC3 promoter were responsible for decreased expression of TUSC3 in GBM. Finally, we determined that TUSC3 regulates proliferation and invasion of GBM cells by inhibiting the activity of the Akt signaling pathway.
Insights
Tumor suppressor candidate 3 (TUSC3) is downregulated in glioblastoma multiforme (GBM). Restoring TUSC3 inhibits GBM cell growth and invasion by affecting the Akt pathway.
Area of Science:
- Neuro-oncology
- Molecular biology
- Cancer genetics
Background:
- Glioblastoma multiforme (GBM) is an aggressive human brain tumor with poorly understood mechanisms.
- Tumor suppressor candidate 3 (TUSC3) is implicated in various cancers but its role in GBM was uncharacterized.
- TUSC3 is involved in protein N-glycosylation and acts as a potential tumor suppressor.
Purpose of the Study:
- To investigate the role of TUSC3 in glioblastoma multiforme.
- To determine the molecular mechanisms underlying TUSC3 dysregulation in GBM.
- To explore TUSC3's impact on GBM cell behavior and signaling pathways.
Main Methods:
- Quantitative analysis of TUSC3 expression in GBM tissues and cell lines.
- Assessment of TUSC3's effect on GBM cell proliferation and invasion.
- Analysis of TUSC3 promoter methylation.
- Investigation of TUSC3's influence on the Akt signaling pathway.
Main Results:
- TUSC3 expression is significantly downregulated in GBM tissues and cells.
- Overexpression of TUSC3 suppressed GBM cell proliferation and invasion.
- Increased promoter methylation correlated with decreased TUSC3 expression in GBM.
- TUSC3 inhibits GBM cell proliferation and invasion by downregulating Akt signaling.
Conclusions:
- TUSC3 functions as a tumor suppressor in glioblastoma multiforme.
- Epigenetic silencing via promoter methylation contributes to TUSC3 downregulation in GBM.
- Targeting TUSC3 or the Akt pathway may offer therapeutic strategies for GBM.
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