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Updated: Feb 28, 2026

Characterization of Functionally Associated miRNAs in Glioblastoma and their Engineering into Artificial Clusters for Gene Therapy
Published on: October 4, 2019
miR-200b inhibits CD133+ glioma cells by targeting the AKT pathway
Aiqun Liu1,2, Qingyun Yu2, Zhongxing Peng2
1Department of Neurology, Jinan University, Guangzhou, Guangdong, 510632, P.R. China.
Abstract:
MicroRNA-200b (miR-200b) is a tumor suppressor in multiple tumor types, including gastric cancer, breast cancer, ovarian cancer and glioma. The biological significance of a known normal and cancer stem cell marker, CD133, remains elusive. The aim of the present study was to identify the function and mechinism of miR-200b in suppressing CD133+ glioma cells. CD133+ glioma cells were sorted by flow cytometry. The expression of miR-200b, Ki67, GAP43, GFAP and CD133 were tested by reverse transcription-quantitative polymerase chain reaction. The binding of miR-200b to prominin 1 (PROM1) was certificated by luciferase reporter assay. Cell proliferation was analyzed by bromodeoxyuridine staining. The protein level of CD133, p-AKT, AKT and Notch1 was detected by western blot analysis. Analysis of glioma samples revealed that CD133 expression is negatively associated with miR-200b. PROM1, which is the gene that codes CD133, was certified to be a target of miR-200b. miR-200b expression inhibited the stemness properties and division of the CD133+ glioma cells. Our results identified a miR-200b/CD133/PI3K/Akt signaling axis, exploring the fundamental role of miR-200b and CD133 in glioma stem cell behavior.
Insights
MicroRNA-200b (miR-200b) acts as a tumor suppressor by inhibiting CD133+ glioma cells. This study reveals miR-200b targets PROM1, suppressing glioma stem cell properties and proliferation.
Area of Science:
- Molecular Biology
- Oncology
- Neuroscience
Background:
- MicroRNA-200b (miR-200b) is a known tumor suppressor.
- CD133 is a marker for normal and cancer stem cells, but its role in glioma is unclear.
- Glioma is a primary brain tumor with significant unmet medical needs.
Purpose of the Study:
- To investigate the function and mechanism of miR-200b in suppressing CD133-positive (CD133+) glioma cells.
- To elucidate the role of the miR-200b/CD133 axis in glioma stem cell behavior.
Main Methods:
- Isolation of CD133+ glioma cells via flow cytometry.
- Quantitative PCR and Western blot analysis to assess gene and protein expression (miR-200b, CD133, PROM1, AKT, Notch1).
- Luciferase reporter assay to confirm miR-200b binding to PROM1; Bromodeoxyuridine staining for cell proliferation analysis.
Main Results:
- Glioma samples showed an inverse correlation between CD133 expression and miR-200b levels.
- Prominin 1 (PROM1), the gene encoding CD133, was validated as a direct target of miR-200b.
- miR-200b significantly inhibited stemness and proliferation in CD133+ glioma cells.
- A miR-200b/CD133/PI3K/Akt signaling pathway was identified.
Conclusions:
- miR-200b functions as a tumor suppressor in glioma by targeting CD133.
- The miR-200b/CD133 interaction regulates glioma stem cell characteristics.
- This study uncovers a critical signaling axis involved in glioma progression and offers potential therapeutic targets.
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