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MiR-136 targets E2F1 to reverse cisplatin chemosensitivity in glioma cells
Wanghao Chen1, Yong Yang, Bo Chen
1Department of Neurosurgery, People's Hospital Affiliated to Jiangsu University, Zhenjiang, China.
Abstract:
MicroRNAs (miRNAs) have gained much attention due to their critical roles in diverse biological events, including tumorigenesis. In this study, we demonstrate that miR-136 is down-regulated in two cohorts of patients with glioma. Furthermore, the low-level expression of miR-136 is significantly associated with a more aggressive and/or poor prognostic phenotype of patients with gliomas. Both gain- and loss-of-function experiments showed that miR-136 expression can reverse cisplatin resistance and enhance the response to cisplatin treatment. Furthermore, we identified a novel direct target of miR-136, the E2F transcription factor 1 (E2F1) oncogene. Depletion of E2F1 recapitulated the tumor-suppressive functions of miR-136, whereas re-expression of E2F1 attenuated the function of miR-136 in glioma cells. Finally, we revealed that miR-136 is inversely correlated with E2F1 expression in human glioma samples. The present study provides functional and mechanistic links between the tumor suppressor miR-136 and the oncogene E2F1 for the development of chemoresistance in human glioma. Our results indicate that targeting of the miR-136/E2F1 axis may provide a promising therapeutic approach to treat glioma.
Insights
MicroRNA 136 (miR-136) is down-regulated in glioma, correlating with poor prognosis. Restoring miR-136 overcomes cisplatin resistance by targeting the E2F1 oncogene, offering a potential therapeutic strategy.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- MicroRNAs (miRNAs) are crucial regulators in biological processes, including cancer development.
- Glioma, a primary brain tumor, presents significant therapeutic challenges, often involving chemoresistance.
Purpose of the Study:
- To investigate the role of miR-136 in glioma pathogenesis and chemoresistance.
- To identify the molecular targets and mechanisms underlying miR-136's function in glioma.
Main Methods:
- Analysis of miR-136 expression in glioma patient cohorts.
- Gain- and loss-of-function experiments to assess miR-136's impact on cisplatin resistance.
- Identification and validation of E2F1 as a direct target of miR-136.
- Correlation analysis of miR-136 and E2F1 expression in clinical samples.
Main Results:
- miR-136 expression is significantly reduced in glioma patients and associated with aggressive disease.
- miR-136 restoration sensitizes glioma cells to cisplatin treatment.
- E2F1 is a direct target of miR-136, and its modulation affects glioma cell behavior.
- Inverse correlation between miR-136 and E2F1 expression in human gliomas.
Conclusions:
- The miR-136/E2F1 axis plays a critical role in glioma chemoresistance.
- Targeting this axis presents a potential therapeutic strategy for improving glioma treatment outcomes.
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