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MiR-22 and miR-205 drive tumor aggressiveness of mucoepidermoid carcinomas of salivary glands [mRNA]

ABSTRACT: We used mRNA expression arrays and integrated analysis to study mucoepidermoid carcinomas (MEC) to identify potential drivers involved with its pathogenesis. Normal salivary glands were used as controls.

ORGANISM(S): Homo sapiens

PROVIDER: GSE169753 | GEO | 2022/03/03

REPOSITORIES: GEO

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miR-22 and miR-205 drive tumor aggressiveness of mucoepidermoid carcinomas of salivary glands [miRNA]

Project description:We used miRNA expression arrays and integrated analysis to study mucoepidermoid carcinomas (MEC) to identify potential drivers involved with its pathogenesis. Normal salivary glands were used as controls.

2022-03-03 | GSE169692 | GEO

miR-22 and miR-205 Drive Tumor Aggressiveness of Mucoepidermoid Carcinomas of Salivary Glands.

Project description:ObjectivesTo integrate mRNA and miRNA expression profiles of mucoepidermoid carcinomas (MECs) and normal salivary gland (NSGs) tissue samples and identify potential drivers.Material and methodsGene and miRNA expression arrays were performed in 35 MECs and six NSGs.ResultsWe found 46 differentially expressed (DE) miRNAs and 3,162 DE mRNAs. Supervised hierarchical clustering analysis of the DE transcripts revealed two clusters in both miRNA and mRNA profiles, which distinguished MEC from NSG samples. The integrative miRNA-mRNA analysis revealed a network comprising 696 negatively correlated interactions (44 miRNAs and 444 mRNAs) involving cell signaling, cell cycle, and cancer-related pathways. Increased expression levels of miR-205-5p and miR-224-5p and decreased expression levels of miR-139-3p, miR-145-3p, miR-148a-3p, miR-186-5p, miR-338-3p, miR-363-3p, and miR-4324 were significantly related to worse overall survival in MEC patients. Two overexpressed miRNAs in MEC (miR-22 and miR-205) were selected for inhibition by the CRISPR-Cas9 method. Cell viability, migration, and invasion assays were performed using an intermediate grade MEC cell line. Knockout of miR-205 reduced cell viability and enhanced ZEB2 expression, while miR-22 knockout reduced cell migration and invasion and enhanced ESR1 expression. Our results indicate a distinct transcriptomic profile of MEC compared to NSG, and the integrative analysis highlighted miRNA-mRNA interactions involving cancer-related pathways, including PTEN and PI3K/AKT.ConclusionThe in vitro functional studies revealed that miR-22 and miR-205 deficiencies reduced the viability, migration, and invasion of the MEC cells suggesting they are potential oncogenic drivers in MEC.

| S-EPMC8864291 | biostudies-literature

miR-22 and miR-205 drive tumor aggressiveness of mucoepidermoid carcinomas of salivary glands

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-03-03 | GSE169754 | GEO

miR-22 and miR-205 drive tumor aggressiveness of mucoepidermoid carcinomas of salivary glands

Project description:miR-22 and miR-205 drive tumor aggressiveness of mucoepidermoid carcinomas of salivary glands

| PRJNA717796 | ENA

miR-22 and miR-205 drive tumor aggressiveness of mucoepidermoid carcinomas of salivary glands [mRNA]

Project description:miR-22 and miR-205 drive tumor aggressiveness of mucoepidermoid carcinomas of salivary glands [mRNA]

| PRJNA717800 | ENA

miR-22 and miR-205 drive tumor aggressiveness of mucoepidermoid carcinomas of salivary glands [miRNA]

Project description:miR-22 and miR-205 drive tumor aggressiveness of mucoepidermoid carcinomas of salivary glands [miRNA]

| PRJNA717676 | ENA

High number of chromosomal copy number aberrations inversely relates to t(11;19)(q21;p13) translocation status in Mucoepidermoid Carcinoma of the Salivary Glands

Project description:genomic analysis using arrayCGH to gain insight into chromosomal copy number in mucoepidermoid carcinoma (MEC). Results suggest that two types of MECs can be distinguished: (i) a group of MECs without t(11;19)(q21;p13) translocation with many copy number aberrations (> 6), independent of histological grade, and (ii) a group of MECs with the t(11;19)(q21;p13) translocation with no or a few copy number aberrations (<6 ) with two exceptions classified as low and intermediate grade.

2017-11-01 | GSE87353 | GEO

Whole-Exome Sequencing of Salivary Gland Mucoepidermoid Carcinoma

Project description:Mucoepidermoid carcinoma (MEC) is the most common salivary gland malignancy. To explore the genetic origins of MEC, we performed systematic genomic analyses of these tumors.Experimental DesignWhole-exome sequencing and gene copy number analyses were performed for 18 primary cancers with matched normal tissue. Fluorescence in situ hybridization (FISH) was used to determine the presence or absence of the MECT1-MAML2 translocation in 17 tumors.ResultsTP53 was the most commonly mutated gene in MEC (28%), and mutations were found only in intermediate- and high-grade tumors. Tumors with TP53 mutations had more mutations overall than tumors without TP53 mutations (p=0.006). POU6F2 was the second most frequently mutated gene, found in three low-grade MECs with the same in-frame deletion. Somatic alterations in IRAK1, MAP3K9, ITGAL, ERBB4, OTOGL, KMT2C, and OBSCN were identified in at least two of the 18 tumors sequenced. FISH analysis confirmed the presence of the MECT1-MAML2 translocation in 15 of 17 tumors (88%).ConclusionsThrough these integrated genomic analyses, MECT1-MAML2 translocation and somatic TP53 and POU6F2 mutations appear to be the main drivers of mucoepidermoid carcinoma.

| EGAS00001002811 | EGA

Identification of the CREB-regulated transcriptional program in human mucoepidermoid carcinoma cells

2015-10-30 | GSE49673 | GEO

Identification of the CREB-regulated transcriptional program in human mucoepidermoid carcinoma cells

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 contribution of the transcription factor CREB to mediate the fusion target gene expression, gene expression profiling analysis were performed in two salivary gland tumor cell lines (including fusion-positive H3118 MEC cells and fusion-negative HSY parotid adenocarcinoma cells) before and after CREB knockdown. This study demonstrated that CRTC1-MAML2 co-activation of CREB is a major mechanism underlying CRTC1-MAML2-mediated transcriptional regulation. Two salivary gland tumor cell lines were used in this study, including fusion-positive H3118 MEC cells and fusion-negative HSY parotid adenocarcinoma cells. The CREB knock down was performed with three biological replicates for each group. Both fusion-positive MEC H3118 cells and fusion-negative parotid adenocarcinoma HSY cells were stably transduced with pLKO.1-based shRNA targeting luciferase gene (shLuc, control) or CREB (shCREB). The cells were independently cultured and RNAs were then harvested 72 hours after transduction for microarray analysis.

2015-10-30 | E-GEOD-49673 | biostudies-arrayexpress

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