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NGS-based miRNome reveals regulation in the miR-34/miR-449 cluster targetome in sinonasal cancers.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE192596 | GEO | 2023/12/28

REPOSITORIES: GEO

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NGS-based miRNome reveals regulation in the miR-34/miR-449 cluster targetome in sinonasal cancers [miRNA-seq]

Project description:Using NGS-based miRNome, followed by AGO2-RIP-seq, the miR-34c and miR-449a and their direct targets were identified as factors involved in the development and progression of sinonasal cancers (SNCs). Both miR-34c and miR-449a were independent prognostic biomarkers and were associated with patient outcome.

2023-12-28 | GSE192595 | GEO

NGS-based miRNome reveals regulation in the miR-34/miR-449 cluster targetome in sinonasal cancers [RIP-seq]

2023-12-28 | GSE192594 | GEO

NGS-based miRNome reveals regulation in the miR-34/miR-449 cluster targetome in sinonasal cancers.

Project description:NGS-based miRNome reveals regulation in the miR-34/miR-449 cluster targetome in sinonasal cancers.

| PRJNA792155 | ENA

NGS-based miRNome reveals regulation in the miR-34/miR-449 cluster targetome in sinonasal cancers [RIP-seq]

Project description:NGS-based miRNome reveals regulation in the miR-34/miR-449 cluster targetome in sinonasal cancers [RIP-seq]

| PRJNA792157 | ENA

NGS-based miRNome reveals regulation in the miR-34/miR-449 cluster targetome in sinonasal cancers [miRNA-seq]

Project description:NGS-based miRNome reveals regulation in the miR-34/miR-449 cluster targetome in sinonasal cancers [miRNA-seq]

| PRJNA792156 | ENA

miR-34/449 miRNAs are required for motile ciliogenesis by repressing cp110.

Project description:The mir-34/449 family consists of six homologous miRNAs at three genomic loci. Redundancy of miR-34/449 miRNAs and their dominant expression in multiciliated epithelia suggest a functional significance in ciliogenesis. Here we report that mice deficient for all miR-34/449 miRNAs exhibited postnatal mortality, infertility and strong respiratory dysfunction caused by defective mucociliary clearance. In both mouse and Xenopus, miR-34/449-deficient multiciliated cells (MCCs) exhibited a significant decrease in cilia length and number, due to defective basal body maturation and apical docking. The effect of miR-34/449 on ciliogenesis was mediated, at least in part, by post-transcriptional repression of Cp110, a centriolar protein suppressing cilia assembly. Consistent with this, cp110 knockdown in miR-34/449-deficient MCCs restored ciliogenesis by rescuing basal body maturation and docking. Altogether, our findings elucidate conserved cellular and molecular mechanisms through which miR-34/449 regulate motile ciliogenesis.

| S-EPMC4119886 | biostudies-literature

miR-34/449 control apical actin network formation during multiciliogenesis through small GTPase pathways.

Project description:Vertebrate multiciliated cells (MCCs) contribute to fluid propulsion in several biological processes. We previously showed that microRNAs of the miR-34/449 family trigger MCC differentiation by repressing cell cycle genes and the Notch pathway. Here, using human and Xenopus MCCs, we show that beyond this initial step, miR-34/449 later promote the assembly of an apical actin network, required for proper basal bodies anchoring. Identification of miR-34/449 targets related to small GTPase pathways led us to characterize R-Ras as a key regulator of this process. Protection of RRAS messenger RNA against miR-34/449 binding impairs actin cap formation and multiciliogenesis, despite a still active RhoA. We propose that miR-34/449 also promote relocalization of the actin binding protein Filamin-A, a known RRAS interactor, near basal bodies in MCCs. Our study illustrates the intricate role played by miR-34/449 in coordinating several steps of a complex differentiation programme by regulating distinct signalling pathways.

| S-EPMC4595761 | biostudies-literature

Motile cilia of the male reproductive system require miR-34/miR-449 for development and function to generate luminal turbulence.

Project description:Cilia are cell-surface, microtubule-based organelles that project into extracellular space. Motile cilia are conserved throughout eukaryotes, and their beat induces the flow of fluid, relative to cell surfaces. In mammals, the coordinated beat of motile cilia provides highly specialized functions associated with the movement of luminal contents, as seen with metachronal waves transporting mucus in the respiratory tract. Motile cilia are also present in the male and female reproductive tracts. In the female, wave-like motions of oviductal cilia transport oocytes and embryos toward the uterus. A similar function has been assumed for motile cilia in efferent ductules of the male-i.e., to transport immotile sperm from rete testis into the epididymis. However, we report here that efferent ductal cilia in the male do not display a uniform wave-like beat to transport sperm solely in one direction, but rather exert a centripetal force on luminal fluids through whip-like beating with continual changes in direction, generating turbulence, which maintains immotile spermatozoa in suspension within the lumen. Genetic ablation of two miRNA clusters (miR-34b/c and -449a/b/c) led to failure in multiciliogenesis in murine efferent ductules due to dysregulation of numerous genes, and this mouse model allowed us to demonstrate that loss of efferent duct motile cilia causes sperm aggregation and agglutination, luminal obstruction, and sperm granulomas, which, in turn, induce back-pressure atrophy of the testis and ultimately male infertility.

| S-EPMC6397547 | biostudies-literature

Control of multiciliogenesis by miR-34/449 in the male reproductive tract through enforcing cell cycle exit.

Project description:Multiciliated cells (MCCs) are terminally differentiated postmitotic cells that possess hundreds of motile cilia on their apical surface. Defects in cilia formation are associated with ciliopathies that affect many organs. In this study, we tested the role and mechanism of the miR-34/449 family in the regulation of multiciliogenesis in EDs using an miR-34b/c-/-; miR-449-/- double knockout (dKO) mouse model. MiR-34b/c and miR-449 depletion led to a reduced number of MCCs and abnormal cilia structure in the EDs starting from postnatal day (P)14. However, abnormal MCC differentiation in the dKO EDs could be observed as early as P7. RNA-seq analyses revealed that the aberrant development of MCCs in the EDs of dKO mice was associated with the upregulation of genes involved in cell cycle control. Using a cyclin-dependent kinase inhibitor to force cell cycle exit promoted MCC differentiation, and partially rescued the defective multiciliogenesis in the EDs of dKO mice. Taken together, our results suggest that miR-34b/c and miR-449 play an essential role in multiciliogenesis in EDs by regulating cell cycle exit.

| S-EPMC8182409 | biostudies-literature

Characterizing isomiR variants within the microRNA-34/449 family.

Project description:miR-34/449 microRNAs are conserved regulators of multiciliated cell differentiation. Here, we evidence and characterize expression of two isomiR variant sequences from the miR-34/449 family in human airway epithelial cells. These isomiRs differ from their canonical counterparts miR-34b and miR-449c by one supplemental uridine at their 5'-end, leading to a one-base shift in their seed region. Overexpression of canonical miR-34/449 or 5'-isomiR-34/449 induces distinct gene expression profiles and biological effects. However, some target transcripts and functional activities are shared by both canonical microRNAs and isomiRs. Indeed, both repress important targets that result in cell cycle blockage and Notch pathway inhibition. Our findings suggest that 5'-isomiR-34/449 may represent additional mechanisms by which miR-34/449 family finely controls several pathways to drive multiciliogenesis.

| S-EPMC5363356 | biostudies-literature

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