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| Status |
Public on Apr 21, 2014 |
| Title |
Identification of CRTC1-MAML2/MAML2-regulated transcriptional program in H3118 cells |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by array
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| Summary |
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.
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| Overall design |
The fusion-positive H3118 MEC cells were used in this study. The fusion 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 for fusion and MAML2 knock down, 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 the knockdown of MAML2 and CRTC1-MAML2 fusion in fusion-positive H3118 cells.
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| Contributor(s) |
Chen J, Li JL, Griffin JD, Wu L |
| Citation(s) |
23975434 |
| |
| Submission date |
May 02, 2013 |
| Last update date |
Jul 11, 2024 |
| Contact name |
Lizi Wu |
| Organization name |
University of Florida
|
| Street address |
2033 Mowry Road
|
| City |
Gainesville |
| State/province |
FL |
| ZIP/Postal code |
32610 |
| Country |
USA |
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| Platforms (1) |
| GPL570 |
[HG-U133_Plus_2] Affymetrix Human Genome U133 Plus 2.0 Array |
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| Samples (4)
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| GSM1132852 |
H3118 CRTC1-MAML2/MAML2 knock-down, biological rep1 |
| GSM1132853 |
H3118 CRTC1-MAML2/MAML2 knock-down, biological rep2 |
| GSM1132854 |
H3118 control, biological rep1 |
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| This SubSeries is part of SuperSeries: |
| GSE59795 |
CRTC1-MAML2 fusion oncogene-induced transcriptional program is regulated by CREB-dependent and -independent mechanisms |
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| Relations |
| BioProject |
PRJNA201048 |
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