Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA214696 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Identification of LINC00473-regulated transcriptional program in human mucoepidermoid carcinoma
| PRJNA323501 | ENA
Project description:Identification of MAML2 regulated transcriptional program in HSY cells
| PRJNA245227 | ENA
Project description:Mucoepidermoid carcinomas (MEC) is the most common salivary gland malignancy. To date, advanced and nonresectable MEC have poor prognosis and no effective treatment. The CRTC1-MAML2 fusion oncogene, which is associated with more than 50% of MEC, consists of the N-terminal CREB-binding domain of the CREB transcriptional co-activator CRTC1 and the C-terminal transcriptional activation domain of the Notch transcriptional co-activator MAML2. CRTC1-MAML2 fusion was found to interact with CREB and constitutively activate their transcriptional targets. To investigate the genes and pathways regulated by CRTC1-MAML2 fusion oncogene, gene expression profiling analysis were performed in human fusion-positive MEC cells before and after knockdown of both CRTC1-MAML2 and MAML2 as well as in human fusion-negative salivary gland cancer cells before and after MAML2 knockdown only. This study revealed specific transcriptional program induced by the CRTC1-MAML2 fusion oncogene, which potentially mediates CRC1-MAML2 functions in MEC initiation and maintenance. The information will be useful for developing new approaches to block CRTC1-MAML2 fusion-expressing MEC.
2015-10-30 | GSE57022 | GEO
Project description:Mucoepidermoid carcinomas (MEC) is the most common salivary gland malignancy. To date, advanced and nonresectable MEC have poor prognosis and no effective treatment. The CRTC1-MAML2 fusion oncogene, which is associated with more than 50% of MEC, consists of the N-terminal CREB-binding domain of the CREB transcriptional co-activator CRTC1 and the C-terminal transcriptional activation domain of the Notch transcriptional co-activator MAML2. CRTC1-MAML2 fusion was found to interact with CREB and constitutively activate their transcriptional targets. To investigate the genes and pathways regulated by CRTC1-MAML2 fusion oncogene, gene expression profiling analysis were performed in human fusion-positive MEC cells before and after knockdown of both CRTC1-MAML2 and MAML2 as well as in human fusion-negative salivary gland cancer cells before and after MAML2 knockdown only. This study revealed specific transcriptional program induced by the CRTC1-MAML2 fusion oncogene, which potentially mediates CRC1-MAML2 functions in MEC initiation and maintenance. The information will be useful for developing new approaches to block CRTC1-MAML2 fusion-expressing MEC.
2014-04-21 | GSE46580 | GEO
Project description:Identification of CRTC1-MAML2/MAML2-regulated transcriptional program in H3118 cells
| PRJNA201048 | ENA
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
2011-02-19 | GSE20463 | GEO
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression. Two-condition experiment, Normoxic MSCs vs. Hypoxic MSCs.
2011-02-19 | E-GEOD-20463 | biostudies-arrayexpress
Project description:Mucoepidermoid carcinomas (MEC) is the most common salivary gland malignancy. To date, advanced and nonresectable MEC have poor prognosis and no effective treatment. The CRTC1-MAML2 fusion oncogene, which is associated with more than 50% of MEC, consists of the N-terminal CREB-binding domain of the CREB transcriptional co-activator CRTC1 and the C-terminal transcriptional activation domain of the Notch transcriptional co-activator MAML2. CRTC1-MAML2 fusion was found to interact with CREB and constitutively activate their transcriptional targets. To investigate the genes and pathways regulated by CRTC1-MAML2 fusion oncogene, gene expression profiling analysis were performed in human fusion-positive MEC cells before and after knockdown of both CRTC1-MAML2 and MAML2 as well as in human fusion-negative salivary gland cancer cells before and after MAML2 knockdown only. This study revealed specific transcriptional program induced by the CRTC1-MAML2 fusion oncogene, which potentially mediates CRC1-MAML2 functions in MEC initiation and maintenance. The information will be useful for developing new approaches to block CRTC1-MAML2 fusion-expressing MEC. The fusion-negative HSY parotid adenocarcinoma cells were used in this study. The MAML2 knockdown was performed with two biological replicates for each group. We utilized pSuperRetro-based retroviruses that express shRNA targeting the MAML2 TAD as well as GFP, and the retroviruses express shRNA targeting luciferase gene (shLuc) and GFP for the control. Cells were infected with retroviruses and cultured for 72 hours. FACS sorting was performed to obtain GFP-positive cells and thus enrich shRNA-expressing cells. RNA was subsequently harvested for microarray analysis. The shMAML2 retroviruses caused MAML2 knockdown in fusion-negative HSY cells.
2015-10-30 | E-GEOD-57022 | biostudies-arrayexpress
Project description:Mucoepidermoid carcinomas (MEC) is the most common salivary gland malignancy. To date, advanced and nonresectable MEC have poor prognosis and no effective treatment. The CRTC1-MAML2 fusion oncogene, which is associated with more than 50% of MEC, consists of the N-terminal CREB-binding domain of the CREB transcriptional co-activator CRTC1 and the C-terminal transcriptional activation domain of the Notch transcriptional co-activator MAML2. CRTC1-MAML2 fusion was found to interact with CREB and constitutively activate their transcriptional targets. To investigate the genes and pathways regulated by CRTC1-MAML2 fusion oncogene, gene expression profiling analysis were performed in human fusion-positive MEC cells before and after knockdown of both CRTC1-MAML2 and MAML2 as well as in human fusion-negative salivary gland cancer cells before and after MAML2 knockdown only. This study revealed specific transcriptional program induced by the CRTC1-MAML2 fusion oncogene, which potentially mediates CRC1-MAML2 functions in MEC initiation and maintenance. The information will be useful for developing new approaches to block CRTC1-MAML2 fusion-expressing MEC. The fusion-positive H3118 MEC cells were used in this study. The fusion knockdown was performed with two biological replicates for each group. Since we are unable to obtain any shRNA that causes specific knockdown of CRTC1-MAML2, we utilized pSuperRetro-based retroviruses that express shRNA targeting the MAML2 TAD as well as GFP for fusion knock down, and the retroviruses express shRNA targeting luciferase gene (shLuc) and GFP for the control. Cells were infected with retroviruses and cultured for 48 hours. FACS sorting was performed to obtain GFP-positive cells and thus enrich shRNA-expressing cells. RNA was subsequently harvested for microarray analysis. The shMAML2 retroviruses caused the knockdown of MAML2 and CRTC1-MAML2 fusion in fusion-positive H3118 cells.
2014-04-21 | E-GEOD-46580 | biostudies-arrayexpress