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Updated: Jun 25, 2025
Analysis of Retinoic Acid-induced Neural Differentiation of Mouse Embryonic Stem Cells in Two and Three-dimensional Embryoid Bodies
Published on: April 22, 2017
Arsenic Trioxide Induces Retinoic Acid-Related Orphan Receptor Beta and Blocks the WNT Pathway to Inhibit Stemness in
Dacheng Ding1, Kaiming Gao1, Xuebin Zhang2
1Department of Neurosurgery, Tianjin Huanhu Hospital.
Abstract:
Glioblastoma (GBM) is a malignant primary brain tumor and an essential contributor to morbidity and mortality globally. Arsenic trioxide (ATO) exerts specific roles in preventing tumor growth. This study investigated the role of ATO in GBM cell behaviors and stemness. The effects of ATO on the malignant behavior of GBM cells, tumor stemness, and epithelial-mesenchymal transition (EMT) factors in mouse tumor tissues were explored. Targets of ATO in GBM were predicted using multiple databases. Subsequently, the expression of retinoic acid-related orphan receptor beta (RORB), WNT-1, β-Catenin, and c-Myc expression were examined in GBM cells before and after ATO treatment.ATO inhibited the malignant behavior of GBM cells in vitro and slowed down the GBM growth in vivo by inhibiting the stemness. The inhibitory effect of ATO on GBM was achieved by promoting RORB levels and strengthening the antagonism to β-Catenin to inhibit Wnt signaling, thus inhibiting tumor growth. Collectively, ATO induced RORB levels in GBM cells and strengthened the antagonistic effect on β-Catenin, thus inhibiting WNT signaling and tumor growth.
Insights
Arsenic trioxide (ATO) inhibits glioblastoma (GBM) growth by targeting cancer stemness. It increases RORB levels and blocks Wnt signaling, reducing tumor progression.
Area of Science:
- Neuro-oncology
- Molecular Biology
- Cancer Research
Background:
- Glioblastoma (GBM) is a highly aggressive primary brain tumor with poor prognosis.
- Arsenic trioxide (ATO) has demonstrated anti-tumor properties.
- Understanding ATO's mechanism in GBM is crucial for developing new therapies.
Purpose of the Study:
- To investigate the effects of ATO on GBM cell behavior, stemness, and epithelial-mesenchymal transition (EMT).
- To identify and validate ATO's molecular targets in GBM.
- To elucidate the signaling pathways modulated by ATO in GBM.
Main Methods:
- In vitro assays to assess GBM cell behavior and stemness.
- In vivo studies using mouse tumor models.
- Bioinformatic prediction of ATO targets using multiple databases.
- Quantitative analysis of key protein and gene expression (RORB, WNT-1, β-Catenin, c-Myc).
Main Results:
- ATO inhibited GBM cell proliferation and invasion in vitro.
- ATO treatment reduced tumor growth and stemness in vivo.
- ATO upregulated retinoic acid-related orphan receptor beta (RORB) expression.
- ATO antagonized β-Catenin, thereby inhibiting Wnt signaling and downstream targets like c-Myc.
Conclusions:
- ATO effectively inhibits GBM malignant behavior and stemness.
- The anti-GBM effects of ATO are mediated by RORB induction and Wnt/β-Catenin pathway inhibition.
- ATO represents a potential therapeutic agent for glioblastoma.
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