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MicroRNA-138 Suppresses Glioblastoma Proliferation through Downregulation of CD44 (NanoString)

ABSTRACT: MicroRNA-138 Suppresses Glioblastoma Proliferation through Downregulation of CD44 (NanoString)

PROVIDER: PRJNA698613 | ENA |

REPOSITORIES: ENA

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MicroRNA-138 Suppresses Glioblastoma Proliferation through Downregulation of CD44

Project description:MicroRNA-138 Suppresses Glioblastoma Proliferation through Downregulation of CD44

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MicroRNA-138 Suppresses Glioblastoma Proliferation through Downregulation of CD44

Project description:MicroRNA-138 Suppresses Glioblastoma Proliferation through Downregulation of CD44

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MicroRNA-138 Suppresses Glioblastoma Proliferation through Downregulation of CD44 (NanoString)

Project description:100 ng of total RNA was processed with the Human v3 miRNA Expression Assay using NanoString nCounter system (NanoString, USA). Expression of individual miRNA was measured by quantitative real-time PCR with TaqMan miRNA Expression kit (Applied Biosystems, Thermo Fisher Scientific, USA).

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MicroRNA-138 suppresses glioblastoma proliferation through downregulation of CD44.

Project description:Tumor suppressive microRNAs (miRNAs) are increasingly implicated in the development of anti-tumor therapy by reprogramming gene network that are aberrantly regulated in cancer cells. This study aimed to determine the therapeutic potential of putative tumor suppressive miRNA, miR-138, against glioblastoma (GBM). Whole transcriptome and miRNA expression profiling analyses on human GBM patient tissues identified miR-138 as one of the significantly downregulated miRNAs with an inverse correlation with CD44 expression. Transient overexpression of miR-138 in GBM cells inhibited cell proliferation, cell cycle, migration, and wound healing capability. We unveiled that miR-138 negatively regulates the expression of CD44 by directly binding to the 3' UTR of CD44. CD44 inhibition by miR-138 resulted in an inhibition of glioblastoma cell proliferation in vitro through cell cycle arrest as evidenced by a significant induction of p27 and its translocation into nucleus. Ectopic expression of miR-138 also increased survival rates in mice that had an intracranial xenograft tumor derived from human patient-derived primary GBM cells. In conclusion, we demonstrated a therapeutic potential of tumor suppressive miR-138 through direct downregulation of CD44 for the treatment of primary GBM.

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