Intronic miRNA-641 controls its host Gene's pathway PI3K/AKT and this relationship is dysfunctional in glioblastoma multiforme.

摘要: MicroRNAs have established their role as important regulators of the epigenome. A considerable number human miRNA genes are found in intronic regions protein-coding host genes, many cases adopting regulatory circuitry. However, emerging evidence foreshadows an unprecedented importance for this relationship: Intronic miRNAs may protect cell from overactivation respective pathway, a setting that trigger tumor development. AKT2 is well-known proto-oncogene central to PI3K/AKT pathway. This pathway known promote growth and survival, especially glioblastoma. Its miRNA, hsa-miR-641, scarcely investigated, however. We hypothesized miR-641 regulates its regulation become dysfunctional indeed expression differs significantly between GBM tissue normal brain samples, transfection glioma cells with antagonizes Combining clinical cultures, biomolecular methods, we could show doesn't affect AKT2's levels, but down-regulates kinases necessary AKT2-activation, thereby affecting functional state. also identified NFAT5 regulated factor these subsequently activate AKT2. In summary, our study first draws connecting line implication glioblastoma