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RNA-seq analysis of glioblastoma stem cells where MEOX2 expression was knocked down by shRNAs

ABSTRACT: RNA-seq analysis of glioblastoma stem cells where MEOX2 expression was knocked down by shRNAs

PROVIDER: PRJNA803464 | ENA |

REPOSITORIES: ENA

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RNA-seq analysis of glioblastoma stem cells where MEOX2 expression was knocked down by shRNAs

Project description:The most widely accepted hypothesis about glioblastoma onset indicates glioblastoma stem-like cells (GSCs) as the cells of origin, also responsible for the high chemo- and radio-resistance of this tumor and of its recurrence. MEOX2 is a transcription factor overexpressed in glioblastoma, whose expression is negatively correlated to patients’ survival. Starting from our observation that MEOX2 expression is strongly enhanced in six GSC lines we tested, we performed shRNA-mediated knock-down experiments in two different GSC lines, and found that MEOX2 depletion inhibits their self-renewal and growth ability, and increases the apoptotic cell death. By a deep transcriptome analysis, we identified a core group of genes modulated in response to MEOX2 knock-down. Among these genes, the repressed ones are largely enriched in genes involved in the hypoxic response and in the glycolytic pathway, two strictly related pathways which contribute to the resistance of high grade gliomas to therapies.

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MEOX2 homeobox gene promotes growth of malignant gliomas [RNA-Seq]

Project description:Glioblastoma (GBM) is an aggressive tumor that frequently exhibits gain of chromosome 7, loss of chromosome 10 and aberrantly activated RTK signaling pathways. Here, we identify mesenchymal homeobox 2 (MEOX2) as a salient oncogenic transcription factor candidate with increased expression in GBMs. Our results suggest that MEOX2 can enhance ERK signaling through a feed-forward mechanism. We show that MEOX2 overexpression can lead to increased growth in bona fide GBM implantation models and cooperates with loss of p53 and PTEN in cerebral organoid models of human malignant gliomas to induce cell proliferation. Furthermore, using high-throughput genomics, we identify transcriptional target genes of MEOX2 in patient-derived GBM tumorsphere models and a fresh frozen GBM tumor.

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MEOX2-mediated regulation of Cathepsin S promotes cell proliferation and motility in glioma.

Project description:Nuclear transcription factor Mesenchyme Homeobox 2 (MEOX2) is a homeobox gene that is originally discovered to suppress the growth of vascular smooth muscle and endothelial cells. However, whether or not it is connected to cancer is yet unknown. Here, we report that MEOX2 functions as a tumor-initiating element in glioma. Bioinformatic analyses of public databases and investigation of MEOX2 expression in patients with glioma demonstrated that MEOX2 was abundant at both mRNA and protein levels in glioma. MEOX2 expression was shown to be inversely linked with the prognosis of glioma patients. MEOX2 inhibition changed the morphology of glioma cells, inhibited cell proliferation and motility, whereas had no effect on cell apoptosis. Besides, silencing of MEOX2 also hampered the epithelial-mesenchymal transition (EMT), focal adhesion maturation, and F-actin assembly. Overexpression of MEOX2 exhibited opposite effects. Importantly, RNA-seq, ChIP assay, and luciferase reporter assay revealed Cathepsin S (CTSS) as a novel transcriptional target of MEOX2 in glioma cells. Consistently, MEOX2 causes glioma tumor development in mice and greatly lowers the survival period of tumor-bearing mice. Our findings indicate that MEOX2 promotes tumorigenesis and progression of glioma partially through the regulation of CTSS. Targeting the MEOX2-CTSS axis might be a promising alternative for the treatment of glioma.

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