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Micronome profiling in 3 pairs of salivary adenoid cystic carcinoma(SACC) and the corresponding nomal salivary gland tissues

ABSTRACT: Micronome profiling in 3 pairs of salivary adenoid cystic carcinoma(SACC) and the corresponding nomal salivary gland tissues

PROVIDER: PRJNA481642 | ENA |

REPOSITORIES: ENA

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Micronome profiling in 3 pairs of salivary adenoid cystic carcinoma(SACC) and the corresponding nomal salivary gland tissues

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.

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Upregulation of lncRNA ADAMTS9-AS2 promotes salivary adenoid cystic carcinoma (SACC) metastasis via miR-143-3p-mediated regulation of PI3K/Akt and MEK/Erk signaling

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.

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

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Project description:Salivary gland adenoid cystic carcinoma (ACC) is a rare malignancy amongst head and neck tumors that is poorly understood on a molecular level. We sought to perform a comprehensive approach for novel oncogene candidate screening under the control of promoter methylation in order to learn more about the molecular basis of this unusual disease. We performed global demethylation of normal salivary gland cell strains using 5-aza-deoxycytidine (5-Aza dC) and trichostatin (TSA). Expression arrays were performed, and the profiles of treated and untreated cells compared. We then used expression microarray analysis of primary ACC and normal salivary gland samples to generate ACC-specific expression profiling. Next, we integrated the two profiles to identify a subset of genes for further validation of decreased methylation in the promoter region in ACC vs normals. Finally, only genes that showed decreased methylation in ACC compared to normal were further validated for mRNA, protein, and promoter methylation levels in a larger ACC cohort.

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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).

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

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Development of gene expression signatures for lncRNA MRPL23-AS1 down regulation

Project description:Lung metastasis is a major factor affecting long-term survival in adenoid cystic carcinoma patients. Here, we report the long noncoding RNA (lncRNA) MRPL23 antisense RNA 1 (MRPL23-AS1), which exhibited remarkably upregulated expression and was correlated with lung metastasis and overall survival in salivary adenoid cystic carcinoma (SACC) patients. To further study which biological process MRPL23-AS1 may be involved in, SACC-LM cells treated with si-control or si-MRPL23-AS1 were subjected to an mRNA microarray. GO analysis was used to identify the significant biological functions of differentially expressed mRNAs.

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