ARMC10 Drives Glioblastoma Progression Through Activating Notch Pathway
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Updated: May 26, 2025

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
Published on: February 28, 2017
Bin Feng1, Taihong Gao1, Lin Chen2
1Department of Neurosurgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Abstract:
This study aimed to check the biological functions and uncover the mechanism of armadillo repeat protein C10 (ARMC10) in glioblastoma (GBM). The expression and potential mechanisms of ARMC10 in GBM were analyzed by bioinformatics analysis. In GBM cells, function-loss experiments were used to evaluate the influences of ARMC10 on cell proliferation, cell invasion, lipid levels, and cell migration by colony formation assay, 5-ethynyl-2'-deoxyuridine staining, cell counting kit-8 assay, transwell assay, BODIPY staining, and wound healing assay. Mouse xenograft models were constructed to validate the influences of ARMC10 in vivo. ARMC10 levels in GBM were upregulated, and patients with low ARMC10 levels displayed a better prognosis. ARMC10 knockdown resulted in a decrease of GBM cell invasion, migration, and proliferation. GSEA showed that ARMC10 was positively associated with the Notch pathway and fatty acid metabolism. ARMC10 knockdown reduced the levels of triglyceride, cholesterol, and lipid, and inhibited the expression of proteins related to fatty acid metabolism and Notch pathway. Moreover, notch receptor 1 (Notch1) overexpression reversed the inhibition of cell proliferation, fatty acid metabolism, and invasion induced by ARMC10 knockdown. In vivo, ARMC10 knockdown suppressed tumor growth. RMC10 knockdown suppressed GBM malignant progression, which had a bearing on Notch pathway.
Insights
Armadillo repeat protein C10 (ARMC10) promotes glioblastoma (GBM) growth by activating the Notch pathway and fatty acid metabolism. Reducing ARMC10 levels inhibits GBM progression and improves patient prognosis.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Glioblastoma (GBM) is an aggressive brain tumor with limited treatment options.
- The role of armadillo repeat protein C10 (ARMC10) in GBM pathogenesis remains largely unexplored.
Purpose of the Study:
- To investigate the biological functions and underlying mechanisms of ARMC10 in glioblastoma.
- To determine the prognostic significance of ARMC10 expression in GBM patients.
Main Methods:
- Bioinformatics analysis of ARMC10 expression and its correlation with GBM.
- In vitro functional assays (proliferation, invasion, migration, lipid levels) using ARMC10 knockdown in GBM cells.
- In vivo studies using mouse xenograft models to assess ARMC10's effect on tumor growth.
- Gene Set Enrichment Analysis (GSEA) to identify associated molecular pathways.
Main Results:
- ARMC10 is upregulated in GBM, and high expression correlates with a poorer prognosis.
- ARMC10 knockdown significantly inhibits GBM cell proliferation, invasion, and migration.
- ARMC10 promotes GBM progression via positive association with the Notch pathway and fatty acid metabolism.
- ARMC10 knockdown reduces lipid levels and inhibits key proteins in fatty acid metabolism and Notch signaling.
- Overexpression of Notch receptor 1 (Notch1) reversed the inhibitory effects of ARMC10 knockdown.
Conclusions:
- ARMC10 plays a crucial role in promoting glioblastoma malignant progression.
- Targeting ARMC10 and its associated Notch pathway and fatty acid metabolism may offer a therapeutic strategy for GBM.
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