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Updated: Apr 30, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
BASI, a potent small molecular inhibitor, inhibits glioblastoma progression by targeting microRNA-mediated β-catenin
Zhen-Dong Shi1, Xiao-Min Qian, Jun-Xia Zhang
1Laboratory of Neuro-Oncology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China; Key Laboratory of Post-Trauma Neuro-Repair and Regeneration in the Central Nervous System, Ministry of Education Tianjin Key Laboratory of Injuries, Variations and Regeneration of the Nervous System, Tianjin, China.
Background And Aims:
The nuclear localization of β-catenin, a mediator of canonical Wnt signaling, has been indicated in a variety of cancers and is frequently related to tumor progression and metastasis. Therefore, targeting β-catenin is an attractive therapeutic strategy for cancers.
Methods:
Herein, we identified a natural, small molecule inhibitor of β-catenin signaling, BASI, and evaluated its therapeutic efficacy both in vitro and in orthotopic mouse models of glioma.
Results:
BASI significantly suppressed proliferation and invasion and induced apoptosis in glioblastoma cells and resulted in the remarkable attenuation of orthotopic tumor growth in vivo. Furthermore, we found that BASI altered the expression of several microRNAs, which mediated the posttranscriptional silencing of β-catenin expression either directly or indirectly through a von Hippel-Lindau (VHL)-mediated β-catenin degradation pattern.
Conclusions:
Taken together, our findings offer preclinical validation of BASI as a promising new type of β-catenin inhibitor with a mechanism of inhibition that has broad potential for the improved treatment of glioblastoma.
Insights
A novel compound, BASI, effectively inhibits beta-catenin (β-catenin) signaling in glioblastoma. This natural molecule suppressed tumor growth and invasion, offering a promising new therapeutic strategy for brain cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapeutics
Background:
- Nuclear localization of beta-catenin (β-catenin) is implicated in various cancers, driving tumor progression and metastasis.
- Targeting β-catenin is a key therapeutic strategy for numerous cancer types.
Purpose of the Study:
- To identify and evaluate a natural small molecule inhibitor of β-catenin signaling.
- To assess the therapeutic efficacy of BASI in glioblastoma models.
Main Methods:
- In vitro studies on glioblastoma cells.
- In vivo evaluation using orthotopic mouse models of glioma.
- Analysis of microRNA expression changes and their role in β-catenin regulation.
Main Results:
- BASI significantly inhibited glioblastoma cell proliferation and invasion while inducing apoptosis.
- Orthotopic tumor growth in vivo was markedly reduced by BASI treatment.
- BASI modulated microRNA expression, leading to posttranscriptional silencing of β-catenin via VHL-mediated degradation.
Conclusions:
- BASI demonstrates preclinical efficacy as a novel β-catenin inhibitor for glioblastoma.
- The compound's mechanism involves microRNA-mediated regulation of β-catenin.
- BASI holds significant potential for advancing glioblastoma treatment strategies.
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