Project description:A human microarray comprising 1658 human genome probes was used to evaluate the specific expression of miRNA between brian glioma stem cells (GSC) and normal neural stem cells(NSC). 2 total RNA samples are analyzed, brian glioma stem cells (GSC) and normal neural stem cells(NSC). cell type: brain glioma stem cells:GSC_1, GSC_2, GSC_3 ; cell line: normal neural stem cells: NSC_1, NSC_2, NSC_3 biological replicate: NSC_1, NSC_2, NSC_3; biological replicate: GSC_1, GSC_2, GSC_3
Project description:Glioblastomas show heterogeneous histological features. These distinct phenotypic states are thought to be associated with the presence of glioma stem cells (GSCs), which are highly tumorigenic and self-renewing sub-population of tumor cells that have different functional characteristics. To investigate Glioblastomas (GBMs) show heterogeneous histological features. These distinct phenotypic states are thought to be originated by the glioma stem cells (GSCs), which are highly tumorigenic and self-renewing sub-population of tumor cells. Notch signaling has been shown to be important for maintenance of GSC population both in vitro and in vivo. A recent study showed that NOTCH -triggered oncogenic activity can be due to not only its ability to regulate coding genes but also long non-coding RNAs (lncRNAs). Here, we investigated the molecular effects of lncRNA in GSC, whose expression is induced by Notch signaling. We searched for downregulated lncRNAs in GSCs by treatment of small interfering RNA (siRNA) targeting Notch1 and JAG1 (si-Notch1 and si-JAG1).
Project description:We report the effects of knockdown of Cancer Stem Cell Specific Distal Enhancer of Sox2 (CASCADES) in human glioma stem cells and fetal neural stem cells.
Project description:Glioblastomas show heterogeneous histological features. These distinct phenotypic states are thought to be associated with the presence of glioma stem cells (GSCs), which are highly tumorigenic and self-renewing sub-population of tumor cells that have different functional characteristics. To investigate gene expression including lncRNA (long non-coding RNA) in GSC, we have performed high-throughput RNA-sequencing (RNA-seq) experiment using Illumina GAIIx.
Project description:Abnormal activation of stemness factors is a crucial signature of cancer stem cells (CSCs), a highly tumorigenic subpopulation in malignant tumors. However, it is unclear whether multi-signaling pathways are activated in CSCs, as like normal stem cells. I would like to report that an inhibitor of differentiation 1 (ID1) activates intracellular multi-signaling involved in proliferation, genesis, and maintenance of glioma stem cells (GSCs) by suppression of Cullin3, an E3 ubiquitin ligase that degrades Cyclin E and components of SHH and WNT signaling. ID1 inhibits BMP-dependent differentiation of GSCs by activation of BMPR2-targeting miR17/20a. ID1HIGH-Cullin3LOW signature correlates with a poor prognosis of GBM patients with a significant association to gene signatures enriched in EGF, WNT, SHH, and BMP signaling. Combinational inhibition of GSC intracellular multi-signaling network increases tumor-bearing mice survival. These results provide insights on molecular and cellular basis of GSC biology, and also suggest necessity of multi-signaling inhibition for GSCs therapy. Two human primary glioma stem cells (GSCs) such as GSC2 and GSC8 were isolated from two individual primary human glioma specimens. The GSCs were directly transfected with pSuper-GFP-ID1-shRNA and pSuper-GFP-Scrambled-shRNA using FuGENE 6 reagent (Roche). The RNA extraction in these cells was used to analyze gene expression.
Project description:A human cDNA microarray comprising 29,187 human genome probes was used to evaluate the transcriptional changes between brian glioma stem cells (GSC) and normal neural stem cells(NSC). There were 6 samples that were analyzed, 3 samples were from glioma stem cells and the other 3 samples form normal neural stem cells were controls. cell type: brain glioma stem cells:GSC_H004, GSC_H005, GSC_H006 ; cell line: normal neural stem cells: NSC_H001, NSC_H002, NSC_H003 biological replicate: NSC_H001, NSC_H002, NSC_H003; biological replicate: GSC_H004, GSC_H005, GSC_H006
Project description:HOX genes encode a family of homeodomain-containing transcription factors involved in the determination of cell fate and identity during embryonic development. They also behave as oncogenes in some malignancies. In this study, we found high expression of the HOXD9 gene transcript in glioma cell lines and human glioma tissues by quantitative real-time PCR. Using immunocytochemistry, we observed HOXD9 protein expression in human brain tumor tissues, including astrocytomas and glioblastomas. To investigate the role of HOXD9 in gliomas, we silenced its expression in the glioma cell line U87 using HOXD9-specific siRNA, and observed decreased cell proliferation, cell cycle arrest, and induction of apoptosis. It was suggested that HOXD9 contributes to both cell proliferation and/or cell survival. The HOXD9 gene was highly expressed in a side population (SP) of SK-MG-1 cells that was previously identified as an enriched-cell fraction of glioma cancer stem-like cells. HOXD9 siRNA treatment of SK-MG-1 SP cells resulted in reduced cell proliferation. Finally, we cultured human glioma cancer stem cells (GCSCs) from patient specimens found with high expression of HOXD9 in GCSCs compared with normal astrocyte cells and neural stem/progenitor cells (NSPCs). Our results suggest that HOXD9 may be a novel marker of GCSCs and cell proliferation and/or survival factor in gliomas and glioma cancer stem-like cells, and a potential therapeutic target. we analyzed the expression and function of HOXD9 in human gliomas and found high expression of HOXD9 in GCSCs. HOXD9 contributes to cell proliferation and/or survival in glioma cells and glioma cancer stem-like cells.