Investigating the circular RNA gene expression characteristics in salivary adenoid cystic carcinoma (SACC) cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE263719 | GEO | 2024/04/18
REPOSITORIES: GEO
Similar Datasets
Project description:To further investigate the circular RNA gene expression characteristics in SACC patients, we utilized the SBC Human (4*180K) ceRNA microarray to identify differential circular RNAs between SACC tissues and normal SMG tissues from the same patient.
2024-04-18 | GSE263601 | GEO
Project description:Neurotropic infiltrative growth and distant metastasis are the main causes of death in salivary adenoid cystic carcinoma (SACC) patients. Long noncoding RNAs (lncRNAs) are involved in many human neoplasms, however their potential roles in SACC are unclear. In our study, we found that ADAMTS9-AS2 was significantly upregulated in SACC patients with metastasis and SACC -LM cells. Moreover, ADAMTS9-AS2 expression was closely associated with the prognosis and distant metastasis in SACC patients. Next, we found that c-myc could specifically bind to the promoter of ADAMTS9-AS2 and activated its transcription. Knockdown of ADAMTS9-AS2 significantly inhibited migration and invasion of SACC cells in vitro and distant lung metastasis in vivo. Furthermore, ADAMTS9-AS2 which mainly expressed in the cytoplasm shared miRNA response elements with ITGA6. Overexpression of ADAMTS9-AS2 competitively bound to miR-143-3p that inhibited ITGA6 from miRNA-mediated degradation, thus activated the activity of PI3K/Akt and MEK/Erk signaling and facilitated SACC metastasis. In summary, ADAMTS9-AS2 promotes migration and invasion in SACC by competing with miR-143-3p. This sheds a new insight into the regulation mechanism of ADAMTS9-AS2 and provides a possible application for the SACC treatment.
2018-07-25 | GSE117575 | GEO
Project description:To screen miRNAs for potential NDRG2 regulation, we performed micronome profiling in 3 pairs of SACC samples and the corresponding normal salivary glands. The sequencing analysis generated approximately 1,000,000 clean reads per sample. All reads were mapped to annotated miRNAs in the miRBase database (version 22), whereas approximately 45% of the clean reads were mapped to mature miRNAs in the database. After applying a stringent filtering criterion to compare the results from SACC tumor tissue and the adjacent normal salivary glands (log2 fold change >1, FDR<0.05), we identified 176 dysregulated miRNAs.
2018-12-25 | GSE117275 | GEO
Project description:MYB-NFIB fusion and NOTCH1 mutation are hallmark genetic events familiar in SACC that promote lung metastasis. However, abnormal expression of MYB and NOTCH1 was also observed in without MYB-NFIB fusion and NOTCH1 mutation. Here, through single-cell RNA sequencing (scRNA-seq) and exome target capture sequencing in two SACC patients without MYB-NFIB fusion and NOTCH1 mutation, we explore in-depth the molecular mechanisms of lung metastasis. Twenty-five types of cells in primary and metastatic tissues were identified via Seurat clustering and categorized into four main stages ranging from near normal to cancer state based on the normal tissue occupancy for each cell cluster. In this context, we identified the Notch signalling pathway enrichment in almost all cancer cells; trajectory and sub-clustering analyses investigated deeply cancer progenitor-like cell clusters in primary tumour-associated lung metastases, in which signature genes enriched in the ‘MYC_TARGETS_V2’ gene set. In vitro, we detected the complexes of the NICD1-MYB-MYC by Co-immunoprecipitation (Co-IP) and incidentally identified retinoic acid (RA) signalling as endogenous antagonists of the ‘MYC_TARGETS_V2’ gene set. Following this, we validate that all-trans retinoic acid (ATRA) reduces the lung metastasis in SACC via correcting erroneous cell differentiation mainly caused by aberrant NOTCH1 or MYB expression. Bioinformatic and immunohistochemical (IHC) analyses of four primary tissues and eleven metastatic lung tissues from patients with SACC suggested that RA system insufficiency partially promotes lung metastasis. These findings imply the value of diagnosis and treatment of the RA system.
2023-03-09 | GSE216913 | GEO
Project description:MYB-NFIB fusion and NOTCH1 mutation are hallmark genetic events familiar in SACC that promote lung metastasis. However, abnormal expression of MYB and NOTCH1 was also observed in without MYB-NFIB fusion and NOTCH1 mutation. Here, through single-cell RNA sequencing (scRNA-seq) and exome target capture sequencing in two SACC patients without MYB-NFIB fusion and NOTCH1 mutation, we explore in-depth the molecular mechanisms of lung metastasis. Twenty-five types of cells in primary and metastatic tissues were identified via Seurat clustering and categorized into four main stages ranging from near normal to cancer state based on the normal tissue occupancy for each cell cluster. In this context, we identified the Notch signalling pathway enrichment in almost all cancer cells; trajectory and sub-clustering analyses investigated deeply cancer progenitor-like cell clusters in primary tumour-associated lung metastases, in which signature genes enriched in the ‘MYC_TARGETS_V2’ gene set. In vitro, we detected the complexes of the NICD1-MYB-MYC by Co-immunoprecipitation (Co-IP) and incidentally identified retinoic acid (RA) signalling as endogenous antagonists of the ‘MYC_TARGETS_V2’ gene set. Following this, we validate that all-trans retinoic acid (ATRA) reduces the lung metastasis in SACC via correcting erroneous cell differentiation mainly caused by aberrant NOTCH1 or MYB expression. Bioinformatic and immunohistochemical (IHC) analyses of four primary tissues and eleven metastatic lung tissues from patients with SACC suggested that RA system insufficiency partially promotes lung metastasis. These findings imply the value of diagnosis and treatment of the RA system.
2023-03-09 | GSE217082 | GEO
Project description:MYB-NFIB fusion and NOTCH1 mutation are hallmark genetic events familiar in SACC that promote lung metastasis. However, abnormal expression of MYB and NOTCH1 was also observed in without MYB-NFIB fusion and NOTCH1 mutation. Here, through single-cell RNA sequencing (scRNA-seq) and exome target capture sequencing in two SACC patients without MYB-NFIB fusion and NOTCH1 mutation, we explore in-depth the molecular mechanisms of lung metastasis. Twenty-five types of cells in primary and metastatic tissues were identified via Seurat clustering and categorized into four main stages ranging from near normal to cancer state based on the normal tissue occupancy for each cell cluster. In this context, we identified the Notch signalling pathway enrichment in almost all cancer cells; trajectory and sub-clustering analyses investigated deeply cancer progenitor-like cell clusters in primary tumour-associated lung metastases, in which signature genes enriched in the ‘MYC_TARGETS_V2’ gene set. In vitro, we detected the complexes of the NICD1-MYB-MYC by Co-immunoprecipitation (Co-IP) and incidentally identified retinoic acid (RA) signalling as endogenous antagonists of the ‘MYC_TARGETS_V2’ gene set. Following this, we validate that all-trans retinoic acid (ATRA) reduces the lung metastasis in SACC via correcting erroneous cell differentiation mainly caused by aberrant NOTCH1 or MYB expression. Bioinformatic and immunohistochemical (IHC) analyses of four primary tissues and eleven metastatic lung tissues from patients with SACC suggested that RA system insufficiency partially promotes lung metastasis. These findings imply the value of diagnosis and treatment of the RA system.
2023-03-09 | GSE217084 | GEO
Project description:MYB-NFIB fusion and NOTCH1 mutation are hallmark genetic events familiar in SACC that promote lung metastasis. However, abnormal expression of MYB and NOTCH1 was also observed in without MYB-NFIB fusion and NOTCH1 mutation. Here, through single-cell RNA sequencing (scRNA-seq) and exome target capture sequencing in two SACC patients without MYB-NFIB fusion and NOTCH1 mutation, we explore in-depth the molecular mechanisms of lung metastasis. Twenty-five types of cells in primary and metastatic tissues were identified via Seurat clustering and categorized into four main stages ranging from near normal to cancer state based on the normal tissue occupancy for each cell cluster. In this context, we identified the Notch signalling pathway enrichment in almost all cancer cells; trajectory and sub-clustering analyses investigated deeply cancer progenitor-like cell clusters in primary tumour-associated lung metastases, in which signature genes enriched in the ‘MYC_TARGETS_V2’ gene set. In vitro, we detected the complexes of the NICD1-MYB-MYC by Co-immunoprecipitation (Co-IP) and incidentally identified retinoic acid (RA) signalling as endogenous antagonists of the ‘MYC_TARGETS_V2’ gene set. Following this, we validate that all-trans retinoic acid (ATRA) reduces the lung metastasis in SACC via correcting erroneous cell differentiation mainly caused by aberrant NOTCH1 or MYB expression. Bioinformatic and immunohistochemical (IHC) analyses of four primary tissues and eleven metastatic lung tissues from patients with SACC suggested that RA system insufficiency partially promotes lung metastasis. These findings imply the value of diagnosis and treatment of the RA system.
2023-03-09 | GSE217083 | GEO
Project description:MYB-NFIB fusion and NOTCH1 mutation are hallmark genetic events familiar in SACC that promote lung metastasis. However, abnormal expression of MYB and NOTCH1 was also observed in without MYB-NFIB fusion and NOTCH1 mutation. Here, through single-cell RNA sequencing (scRNA-seq) and exome target capture sequencing in two SACC patients without MYB-NFIB fusion and NOTCH1 mutation, we explore in-depth the molecular mechanisms of lung metastasis. Twenty-five types of cells in primary and metastatic tissues were identified via Seurat clustering and categorized into four main stages ranging from near normal to cancer state based on the normal tissue occupancy for each cell cluster. In this context, we identified the Notch signalling pathway enrichment in almost all cancer cells; trajectory and sub-clustering analyses investigated deeply cancer progenitor-like cell clusters in primary tumour-associated lung metastases, in which signature genes enriched in the ‘MYC_TARGETS_V2’ gene set. In vitro, we detected the complexes of the NICD1-MYB-MYC by Co-immunoprecipitation (Co-IP) and incidentally identified retinoic acid (RA) signalling as endogenous antagonists of the ‘MYC_TARGETS_V2’ gene set. Following this, we validate that all-trans retinoic acid (ATRA) reduces the lung metastasis in SACC via correcting erroneous cell differentiation mainly caused by aberrant NOTCH1 or MYB expression. Bioinformatic and immunohistochemical (IHC) analyses of four primary tissues and eleven metastatic lung tissues from patients with SACC suggested that RA system insufficiency partially promotes lung metastasis. These findings imply the value of diagnosis and treatment of the RA system. Cells from fresh tumour tissues were isolated for the preparation of single-cell suspensions via the ChromiumTM Single Cell 3’ Solution technique and analysed by BioMiao Biological Technology (Beijing) Co., Ltd.
2023-03-09 | GSE217081 | GEO
Project description:Micronome profiling in 3 pairs of salivary adenoid cystic carcinoma(SACC) and the corresponding nomal salivary gland tissues
| PRJNA481642 | ENA
Project description: Not available
| S-EPMC4818686 | biostudies-literature