Identification of the YAP1-MAML2 fusion-regulated genes in ovarian cancer ES-2 cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE267241 | GEO | 2024/12/18
REPOSITORIES: GEO
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Project description:Identification of the YAP1-MAML2 fusion-regulated genes in ovarian cancer ES-2 cells
| PRJNA1110603 | 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. 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
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:We analyzed the expression profiles of human and mouse meningiomas (driven by NF2 loss, YAP1-MAML2, TRAF7/KLF4/SMO1/AKT1, or constitutively active non-fusion YAP1). We found that YAP1-MAML2 meningiomas resemble NF2mutant tumors and constitutively exert de-regulated YAP1 activity that is dependent on the interaction with TEADs.
2022-09-02 | GSE199549 | GEO
Project description:We analyzed the expression profiles of human and mouse meningiomas (driven by NF2 loss, YAP1-MAML2, TRAF7/KLF4/SMO1/AKT1, or constitutively active non-fusion YAP1). We found that YAP1-MAML2 meningiomas resemble NF2mutant tumors and constitutively exert de-regulated YAP1 activity that is dependent on the interaction with TEADs.
2022-09-02 | GSE199562 | 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:Using high-resolution oligonucleotide arrayCGH, FISH, and RT-PCR we have performed a comprehensive analysis of genomic imbalances, and CRTC1-MAML2 gene fusion status in a series of 28 well characterized mucoepidermoid carcinomas (MECs) with the aims to identify distinct differences in genomic profiles and CRTC1-MAML2 gene fusion status between low- and high-grade MECs.
2012-12-31 | GSE36282 | GEO
Project description:Using high-resolution oligonucleotide arrayCGH, FISH, and RT-PCR we have performed a comprehensive analysis of genomic imbalances, and CRTC1-MAML2 gene fusion status in a series of 28 well characterized mucoepidermoid carcinomas (MECs) with the aims to identify distinct differences in genomic profiles and CRTC1-MAML2 gene fusion status between low- and high-grade MECs. High-resolution aCGH (44K/244K) on fresh frozen and paraffin embedded tissue from 28 well-characterized MECs.
2012-12-31 | E-GEOD-36282 | 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.
2015-10-30 | GSE57022 | GEO
Project description:BackgroundMetaplastic thymoma is a very rare tumor with only a few case reports documented in literature. Hence, its molecular features have not been well explored.Material and methodsSeventeen specimens of metaplastic thymoma were sequenced and retrospectively analyzed by fluorescence in situ hybridization (FISH) and immunohistochemistry in the study. In addition, seven cases of micronodular thymoma with lymphoid stroma and nine cases of type A thymoma were also investigated.ResultsAmong these metaplastic thymomas, fifteen cases showed classical histological features, and two cases displayed characteristic micronodular-like growth patterns. DNA and RNA based next-generation sequencing identified and confirmed highly recurrent Yes Associated Protein 1 (YAP1) - Mastermind Like Transcriptional Coactivator 2 (MAML2) translocation (13/17, 76.5%) in metaplastic thymoma but not in micronodular thymoma with lymphoid stroma (0/7, 0%) and type A thymoma (0/9, 0%). In addition, six nonsense mutations were also detected in the metaplastic thymoma. FISH in microdissection specimens indicated that both epithelioid and spindle cell components harbored YAP1-MAML2 gene rearrangements.ConclusionsOur study explored the genetic alterations in epithelioid and spindle cell components in metaplastic thymoma. Furthermore, YAP1-MAML2 gene rearrangements emerged as a potential diagnostic biomarker helpful for distinguishing metaplastic thymoma from type A and micronodular thymoma with lymphoid stroma.
| S-EPMC8329546 | biostudies-literature