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MiR-205 enhances cisplatin sensitivity of glioma cells by targeting E2F1.

OBJECTIVE
miR-205 has been previously identified as a diagnostic and prognostic factor in glioma. However, its exact functions in glioma remain unclear. The current research aimed to decipher the role of miR-205 in the development of cisplatin resistance in glioma cells.


MATERIALS AND METHODS
miR-205 expressions in both cisplatin sensitive and resistant cell lines were compared by the Real-time PCR method. The dose-response to cisplatin of U87/DDP cells was determined by MTT assay. Cell cycle and apoptosis were determined by flow cytometry, caspase 3/7 activity assay and Western blot assay. The direct repression of E2F1 by miR-205 was confirmed by luciferase assay and Western blot assay.


RESULTS
miR-205 expression was decreased in cisplatin resistant glioma cell lines, and cisplatin treatment led to a decrease of miR-205 in glioma cells. Overexpression of miR-205 in U87/DDP restored its cisplatin sensitivity by enhancing apoptosis and G1/S cell cycle arrest; notably, all these effects were then partially abrogated by E2F1 overexpression. Luciferase assay and Western blot assay confirmed E2F1 as the direct target of miR-205 in U87/DDP cells.


CONCLUSIONS
These findings suggest that down-regulation of miR-205 confers the cisplatin resistance in glioma cells via upregulation of E2F1. It might serve as a candidate for glioma therapy.