Project description:To investigate the effect of gene alteration of Miat and Mtdh in mouse stem-like MB cells. by canonical oncogenic signaling to maintains the self-renewal capacity of a population of tumorigenic stem-like medulloblastoma cells that are resistant to cytotoxic therapy. by canonical oncogenic signaling to maintains the self-renewal capacity of a population of tumorigenic stem-like medulloblastoma cells that are resistant to cytotoxic therapy. Miat and Mtdh cooperate to promote medulloblastoma tumorigenesis and treatment resistance by regulating the biogenesis of a subset of microRNAs that target genes involved in these processes.
Project description:To investigate the effect of gene alteration of Miat in mouse stem-like MB cells. by canonical oncogenic signaling to maintains the self-renewal capacity of a population of tumorigenic stem-like medulloblastoma cells that are resistant to cytotoxic therapy. by canonical oncogenic signaling to maintains the self-renewal capacity of a population of tumorigenic stem-like medulloblastoma cells that are resistant to cytotoxic therapy. Miat and Mtdh cooperate to promote medulloblastoma tumorigenesis and treatment resistance by regulating the biogenesis of a subset of microRNAs that target genes involved in these processes.
Project description:Genome-wide transcriptomic analyses in left ventricles (LVs) from systemic MIAT knockout (KO) mice were performed to identify novel MIAT targets in the heart.
Project description:T helper 17 (Th17) cells protect against fungal and bacterial infections and are implicated in autoimmunity. Several long intergenic noncoding RNAs (lincRNA) are induced during Th17 differentiation, however, their contribution to Th17 differentiation is poorly understood. We discovered a lincRNA myocardial infarction associated transcript (MIAT) to be upregulated early after induction of human Th17 cell differentiation along with an increase in the chromatin accessibility at the gene locus. We found that MIAT deficiency leads to chromatin accessibility at several loci including IL17A promoter.
Project description:MDA-MB-231 cells were treated with PBS, LPS, IL1b, TNFa, IL6, and TGFb respectively and expression profile were assayed by Arraystar human lncRNA array 2.0 We designed this experiment to screen for lncRNAs whose expressions are responsive to inflammatory stimuli.
Project description:MiR-200c is a well-studied miRNA that is involved in stemness, the epithelial-mesenchymal transition, chemoresistance, radioresistance, and invasion/metastasis of various cancer cells. To obtain an overview of the lncRNA/mRNA regulated by miR-200c signaling in breast-cancer cell lines, we performed global lncRNA/mRNA-expression profiling on MDA-MB-231-pGIPZ and MDA-MB-231-miR-200c cells.
Project description:T helper 17 (Th17) cells protect against fungal and bacterial infections and are implicated in autoimmunity. Several long intergenic noncoding RNAs (lincRNA) are induced during Th17 differentiation, however, their contribution to Th17 differentiation is poorly understood. We discovered a lincRNA myocardial infarction associated transcript (MIAT) to be upregulated early after induction of human Th17 cell differentiation along with an increase in the chromatin accessibility at the gene locus. RNA-seq analysis identified genes implicated in Th17 differentiation and functions as MIAT targets. Our data suggests that MIAT contributes to human Th17 differentiation by upregulating several genes implicated in Th17 differentiation.