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

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

PROVIDER: PRJNA717796 | ENA |

REPOSITORIES: ENA

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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

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

Project description: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.

2022-03-03 | GSE169753 | GEO

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

Genes modulated by miR-205 in DU145 prostate cancer cells

Project description:The study was aimed at identifying genes directly or indirectly regulated by miR-205 in the prostate. To this purpose, DU145 prostate cancer cells, which express miR-205 at very low levels, were transfected with miR-205 synthetic precursor and consequent alterations of gene expression analyzed using a microarray approach. Keywords: comparison betweed cells exposed to different miRNA precursors

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Single cell RNA-seq analysis of mouse miR-205 inducible adult back skin

Project description:Through phenotypical study, we found that miR-205 can promote hair growth. The goal of this study is to determine how miR-205 effects epithelial cellular states and how miR-205 promotes hair growth at single cell level.

2023-06-07 | GSE185115 | GEO

Transcriptome analysis in hair follicle stem cells after miR-205 induction in mouse

Project description:Through phenotypical study, we found that miR-205 can promote hair growth. The goals of this study is to identify direct targets of miR-205 in hair follicle stem cells and determine whether and how miR-205 promotes hair growth by activating hair follicle stem cell.

2023-06-07 | GSE185116 | GEO

Identification of miR-205 targets using an RIP-Chip assay with AGO2 antibody

Project description:In this study, the prognostic properties of miR-205 expression levels are investigated in a well-documented prostate cancer cohort. We show that miR-205 is correlated to shortened overall survival, significantly dividing the PCa patients into high and low risk groups. Furthermore, miR-205 is shown to inversely correlate to occurrence of metastases. In situ hybridization is also performed, demonstrating high miR-205 expression in the basal cells of benign prostate tissue glands. A RIP-Chip assay using an AGO2 antibody was implemented and the miR-205 targets identified were found to be enriched in MAPK/ERK, Toll-like receptor and IL-6 signaling pathways. We also found individual targets involved in cancer and androgen receptor signaling. Ectopic levels of miR-205 are shown to decrease the level of androgen receptor both at the mRNA and protein levels in prostate cancer cell lines. This is further corroborated in the prostate cancer cohort were miR-205 expression levels in the prostatic tissues are found to inversely correlate to assessment of androgen receptor (AR) immunostaining and to serum levels of PSA, a protein regulated by AR signaling. The level of miR-205 is also found to be significantly lower in castration resistant prostate cancer patients than in hormone naïve patients. Our data indicates that miR-205 is regulated by androgens and act by different mechanisms in androgen depleted settings, e.g. giving opposite effects on adhesion. Taken together these findings imply that miR-205 might have therapeutic potential especially for the castration resistant and currently untreatable form of prostate cancer.

2013-12-31 | GSE39735 | GEO

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