EOC progression and warrant further and more profound studies of the functional implications of the RUNX transcription factors in EOC tumorigenesis. GBM is one of the most aggressive tumors. Patients usually have a median overall survival of 12-15 
months, due to the high rate of tumor recurrence despite surgical tumor removal and radio-chemotherapy, which highlights the need for more effective therapies. It has been proposed that gliomagenesis initiates in adult neural stem cells or neural precursors that undergo transformation into GBM-initiating cells, which display a stem cell-like behavior. GICs are able to self-renew, express stem cell markers such as CD133 and Nestin, and can generate and propagate tumors in immunodeficient mice. In addition, GICs are highly resistant to current therapies, possibly explaining the frequent tumor relapses. Of note, GICs can be induced to differentiate into mature cells of the main CNS lineages, which lose their stem cell behavior and become more sensitive to certain therapies. As representative examples, differentiation of CD133+ GBM cells with bone morphogenetic protein 4 or using an all-trans retinoic acid based treatment led to inhibition of the tumorigenic potential of these cells and resulted in retardation of GBM growth in mice, as well as in sensitizing cells to radiation and BCNU chemotherapy in the case of ATRA. Furthermore, our group recently discovered that blockade of NF��B pathway promotes terminal differentiation and senescence of GICs both in vitro and in vivo. All these data suggest that induction of differentiation may be a potential therapeutic strategy for GBM. MicroRNAs are small non-coding RNAs that bind to specific sites in the 3��-UTR of their target mRNAs by partial complementarity, subsequently inducing their degradation and/or the inhibition of their translation. miRNAs play a number of different roles in the regulation of stem cell biology, differentiation, and cell identity. For example, miRNAs have been implicated in the transition from neural stem/precursor cells to differentiated neurons. In addition, miRNAs are key players in tumor development, including GBM. Several miRNAs display deregulated PF-4217903 956905-27-4 expression in GBM samples, and some of them have been shown to regulate differentiation of GICs into mature neural-like cells. Accordingly, the use of interfering RNAs aiming to induce GIC differentiation may represent a promising therapeutic approach in malignant gliomas. However, a global analysis of miRNA expression changes occurring during GIC differentiation has not been performed yet. We have recently established several human GIC lines that can be efficiently differentiated into cells expressing astrocytic and neuronal lineage markers in vitro. Using this system, here we performed a microarray-based highthroughput miRNA expression analysis to uncover the dynamic expression changes of miRNAs during GIC differentiation. Our study identified several miRNA and their potential target genes that may play a role in this process. Our work Temozolomide provides for the first time a high-throughput analysis of miRNA expression during differentiation of GICs. This model resembles the clinical conditions in which the therapeutic induction of differentiation of GICs should be achieved more accurately than the ones based on growth factor withdrawal, since the tumor microenvironment is rich in growth factors. Probably due to this methodological difference, we did not confirm previous findings that reported a pro-differentiation role for miR-124 and miR-137 on human GICs. On the contrary, we found that in our miRNA microarray data these miRNAs were expressed at very low levels or none at all. Moreover, Silber et al. also found that the expression of miR-124 and miR-137 was associated with neuronal-like opposed to astrocyte-like differentiation.