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Extracellular Vesicles Containing circMYBL1 Induce CD44 in Adenoid Cystic Carcinoma Cells and Pulmonary Endothelial Cells to Promote Lung Metastasis.

ABSTRACT: Extracellular Vesicles Containing circMYBL1 Induce CD44 in Adenoid Cystic Carcinoma Cells and Pulmonary Endothelial Cells to Promote Lung Metastasis.

PROVIDER: PRJNA1097554 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28589639_1.fastq.gz	Fastqsanger.gz
	SRR28589639_2.fastq.gz	Fastqsanger.gz
	SRR28589640_1.fastq.gz	Fastqsanger.gz
	SRR28589640_2.fastq.gz	Fastqsanger.gz
	SRR28589641_1.fastq.gz	Fastqsanger.gz

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Extracellular Vesicles Containing circMYBL1 Induce CD44 in Adenoid Cystic Carcinoma Cells and Pulmonary Endothelial Cells to Promote Lung Metastasis.

Project description:Adenoid cystic carcinoma (ACC) is a rare malignant epithelial neoplasm that arises in secretory glands and commonly metastasizes to the lungs. MYBL1 is frequently overexpressed in ACC and has been suggested to be a driver of the disease. Here, we identified a circRNA derived from MYBL1 pre-mRNA that accompanied overexpression of MYBL1 in ACC. Overexpression of circMYBL1 was correlated with increased lung metastasis and poor overall survival in ACC patients. Ectopic circMYBL1 overexpression promoted malignant phenotypes and lung metastasis of ACC cells. Mechanistically, circMYBL1 formed a circRNA-protein complex with CCAAT enhancer binding protein beta (CEBPB), which inhibited ubiquitin-mediated degradation and promoted nuclear translocation of CEBPB. In the nucleus, circMYBL1 increased the binding of CEBPB to the CD44 promoter region and enhanced its transcription. In addition, circMYBL1 was enriched in small extracellular vesicles (sEVs) isolated from the plasma of ACC patients. Treatment with sEVs containing circMYBL1 in sEVs enhanced pro-metastatic phenotypes of ACC cells, elevated the expression of CD44 in human pulmonary microvascular endothelial cells (HPMECs), and enhanced the adhesion between HPMECs and ACC cells. Moreover, circMYBL1 encapsulated in sEVs increased the arrest of circulating ACC cells in the lung and enhanced the lung metastatic burden. This data suggests that circMYBL1 is a tumor-promoting circRNA that could serve as a potential biomarker and therapeutic target in ACC.

2024-04-18 | GSE263444 | GEO

ChIP-seq of MYB in adenoid cystic carcinoma (ACC) ACCX11 cells

Project description:Chromatin immunoprecipitation was carried out using an anti-MYB antibody in PDX-derived ACCX11 adenoid cystic carcinoma cells. Input samples were extracted prior to the addition of antibody.

2023-12-01 | E-MTAB-12976 | biostudies-arrayexpress

Spatial transcriptomics of adenoid cystic carcinoma of the lacrimal gland

Project description:We performed spatial transcriptomics of a tumor section from a patient post-treatment with adenoid cystic carcinoma of the lacrimal gland.

2023-07-05 | GSE228685 | GEO

RNA-seq of adenoid cystic carcinoma (ACC) ACCX11 cells compared to normal salivary glands

Project description:PDX-derived ACCX11 adenoid cystic carcinoma cells were compared to normal salivary gland (NSG) controls.

2023-12-01 | E-MTAB-12978 | biostudies-arrayexpress

Gene expression profile at single cell level of a rare seen and young tracheal adenoid cystic carcinoma

Project description:tracheal adenoid cystic carcinoma is one kind of non-small-cell lung cancer with limit treatment options. We used single cell RNA sequencing (scRNA-seq) to analyze the molecular characteristic of tracheal adenoid cystic carcinoma, aiming to recognized this disease deeply and provide potential treatment plan in the future.

2024-10-31 | GSE245170 | GEO

Mutational characterization of adenoid cystic carcinoma

Project description:Mutational characterization of adenoid cystic carcinoma

| PRJNA197420 | ENA

Human adenoid cystic carcinoma vs. human normal lymphocyte

Project description:We analyzed ten adenoid cystic carcinomas of head and neck by array-based comparative genomic hybridization (a-CGH) using DNA chips spotted 4,030 BAC clones. After data smoothing by the adaptive weights smoothing (AWS) procedure with the gain and loss analysis of DNA (GLAD) algorithm, a total of 89 DNA copy number aberrations (DSCNAs) were detected. The frequent (≥30%) DSCNAs were loss of 6q24, 6q25, 8p23, 6q25, and 6q23 and gains of 6q23, 8p23, 9p11-13, and 22q13. High-level gain was detected on 12q12-15 including MDM2 in two cases. These two cases showed immunohistochemically positive status of MDM2 and negative status of p53 and p21. Furthermore, the total number of DSCNAs was significantly greater in ACC with loss of 6q than in other ACC, in ACC without loss of 8p23 than in other ACC, and in ACC with 8p23 gain than in ACC with 8p23 loss, respectively. Though there is a limit in the evidence, a-CGH detected several candidate chromosomal imbalances associated with DSCNA accumulation in ACC. 6q loss, 12q gain aCGH DNA copy number aberrations screening in human cancer adenoid cystic carcinoma (ACC).

2011-08-31 | E-GEOD-22328 | biostudies-arrayexpress

Integrated copy number and transcriptomic profiling reveal novel oncogenic drivers and clinically significant biomarkers in adenoid cystic carcinoma [Affymetrix]

Project description:This experiment investigates global gene expression in adenoid cystic carcinoma (30) and normal salivary gland tissue (7).

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Differential gene expression of adenoid cystic carcinoma of the lacrimal gland compared to normal lacrimal gland

Project description:To identify the transcriptomic signature of adenoid cystic carcinoma of the lacrimal gland (LGACC), we performed RNA sequencing on LGACC tumor samples and normal lacrimal gland samples.

2023-07-05 | GSE228914 | GEO

Xenograft model systems of adenoid cystic carcinoma

Project description:Adenoid cystic carcinoma (ACC) is one of the most common malignancies that arise in the salivary glands, with an incidence of 4.5 per 1,000,000. It can also arise in glandular tissue closely related to salivary glands in the lacrimal gland, nasal passages and tracheobronchial tree, as well as in glands of the breast and vulva. At all of these sites, it is characterized by a distinctive histology of basaloid epithelial cells arranged in cribriform or tubular patterns, usually demonstrating abundant hyaline extracellular matrix secretion and some degree of myoepithelial differentiation. ACC is generally a slow-growing tumor characterized by a protracted clinical course, usually well over 5 years in duration, marked by regional recurrence, distant metastasis and/or spread along peripheral nerves. A recurrent chromosomal translocation, t(6;9)(q23;p21), has been identified in ACC, and recently it has been discovered that in a majority of ACC the MYB gene on chromosome 6 is fused to the 3’ terminus of the NFIB gene on chromosome 9, creating a fusion gene product resulting in increased MYB-related transcriptional activation. Recently it has been determined that most cell lines with attribution of ACC derivation are either contaminants of other cell lines or do not have the characteristic MYB-NFIB translocation. Also, there are no animal models of this histologically and genetically defined tumor type. To address the paucity of experimental and pre-clinical models systems of ACC, we have for several years been establishing xenograft tumor lines from clinical samples of ACC. We describe our experience with these models and their characterization here. Analysis of 12 xenografts of human adenoid cystic carcinoma (ACC) along with 10 samples of ACC directly from humans. Note, that 12 of these samples are paired primary ACC & xenograft ACC from the same individual (6 pairs in total).

2011-05-03 | E-GEOD-28996 | biostudies-arrayexpress

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