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MiR-26b reverses temozolomide resistance via targeting Wee1 in glioma cells
Lixia Wang1, Jingna Su1, Zhe Zhao1
1a The Cyrus Tang Hematology Center and Collaborative Innovation Center of Hematology , Soochow University , Suzhou , China.
Abstract:
Emerging evidence has demonstrated that microRNAs (miRNA) play a critical role in chemotherapy-induced epithelial-mesenchymal transition (EMT) in glioma. However, the underlying mechanism of chemotherapy-triggered EMT has not been fully understood. In the current study, we determined the role of miR-26b in regulation of EMT in stable temozolomide (TMZ)-resistant (TR) glioma cells, which have displayed mesenchymal features. Our results illustrated that miR-26b was significantly downregulated in TR cells. Moreover, ectopic expression of miR-26b by its mimics reversed the phenotype of EMT in TR cells. Furthermore, we found that miR-26b governed TR-mediate EMT partly due to governing its target Wee1. Notably, overexpression of miR-26b sensitized TR cells to TMZ. These findings suggest that upregulation of miR-26b or targeting Wee1 could serve as novel approaches to reverse chemotherapy resistance in glioma.
Insights
MicroRNAs (miRNAs) are key in chemotherapy resistance in glioma. Upregulating miR-26b can reverse this resistance by targeting Wee1, offering new therapeutic strategies for glioma treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) are increasingly recognized for their role in chemotherapy-induced epithelial-mesenchymal transition (EMT) in glioma.
- The precise mechanisms driving chemotherapy resistance in glioma, particularly EMT, remain incompletely understood.
Purpose of the Study:
- To investigate the role of miR-26b in regulating EMT in temozolomide (TMZ)-resistant glioma cells.
- To explore the therapeutic potential of miR-26b in overcoming chemotherapy resistance in glioma.
Main Methods:
- Stable temozolomide (TMZ)-resistant (TR) glioma cells were established and characterized for mesenchymal features.
- Quantitative real-time PCR was used to assess miR-26b expression levels.
- Ectopic expression of miR-26b was achieved using miRNA mimics.
- The target gene Wee1 was identified and its regulation by miR-26b was investigated.
- Sensitivity of TR cells to TMZ after miR-26b overexpression was evaluated.
Main Results:
- miR-26b was significantly downregulated in TR glioma cells compared to sensitive cells.
- Ectopic expression of miR-26b reversed the EMT phenotype in TR cells.
- miR-26b was found to regulate TR-mediated EMT by targeting the Wee1 gene.
- Overexpression of miR-26b sensitized TR cells to TMZ treatment.
Conclusions:
- miR-26b plays a crucial role in suppressing EMT and overcoming TMZ resistance in glioma.
- Targeting Wee1 through miR-26b upregulation presents a promising therapeutic strategy for enhancing chemotherapy efficacy in glioma.
- Further research into miR-26b and Wee1 interactions could lead to novel treatments for chemoresistant glioma.
