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MiR-148a-3p and DDX6 functional link promotes survival of myeloid leukemia cells

ABSTRACT: Post-transcriptional regulation of genes is heavily dependent on the action of miRNAs. miRNAs take part in various cellular processes and have been shown to be crucial in oncogenesis. Identification of miRNA targets is crucial for understanding its functions in different cellular contexts. miR-148a-3p is highly expressed in HCT116 cells and several other cell lines. However, the studies about mRNA targetting activitiy of this miRNA was limited. In this study, we aimed at identifying target repotoire of miR-148a-3p by using HCT116 DROSHA-KO model. We found several genes that are under miR-148a-3p regulation, including several reported targets. We next found the negative association between miR-148a-3p and DDX6, one of the identified gene, in leukemia. We examined DDX6 functions in this cancer and showed that the depletion of DDX6 helps impair leukemia cell growth, promote apoptosis and increase survival rate of transplanted mice. We then identified that DDX6 functions to suppress TXNIP, a well known tumor suppressor in leukemia and various types of cancer. Our findings uncovered the regulation axis between miR-148a-3p/DDX6/TXNIP in leukemia which provides molecular mechanism basis for therapeutic treatment directions.

ORGANISM(S): Homo sapiens

PROVIDER: GSE201905 | GEO | 2022/06/07

REPOSITORIES: GEO

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miR-148a-3p and DDX6 functional link promotes survival of myeloid leukemia cells

Project description:miR-148a-3p and DDX6 functional link promotes survival of myeloid leukemia cells

| PRJNA833443 | ENA

Quantitative Proteomics of miR-148a in gastric cancer cells

Project description:A quantitative proteomics combined with stable isotope labeling was applied to identify the global profile of miR-148a-regulated downstream proteins in AGS cancer cells. For proteomic analysis, cells were treated with miR-148a mimic (Pre-miR-148a) or miR-148a negative control (miR-CTL) and the downstream protein expression level (Pre-miR-148a/miR-CTL) were quantified using iTRAQ approach. Bioinformatics pipeline: The peak list in the resultant MS/MS spectra were generated by Mascot Distiller v2.1.1.0 and searched using Mascot v2.2 against the International Protein Index (IPI) human database (v. 3.64, 84032 sequences). The Mascot search parameters were +-0.1 Da for MS tolerance, +-0.1 Da for MS/MS mass tolerance, allowances for two missed cleavages, and variable modifications of deamidation (NQ), oxidation (M), iTRAQ (N terminal), iTRAQ (K), and MMTS (C). Protein quantitation were calculated using the Multi-Q software v1.6.5.4 with a dynamic range filter of ion count > 30.

2013-07-24 | PXD000190 | Pride

MicroRNA-148a-3p in pericyte-derived extracellular vesicles improves erectile function in diabetic mice by promoting cavernous neurovascular regeneration

Project description:Purpose: To investigate the regulatory role of microRNA (miR)-148a-3p in mouse corpus cavernous pericyte (MCPs)-derived extracellular vesicles (EVs) in the treatment of diabetes-induced erectile dysfunction (ED). Materials and Methods: Mouse corpus cavernous tissue was used for MCPs primary culture and EVs isolation. Small RNA sequencing analysis was performed to assess the type and content of miRs in MCPs-EVs. Four groups of mice were used: control nondiabetic mice and streptozotocin-induced diabetic mice receiving two intracavernous injections (days -3 and 0) of phosphate buffered saline, MCPs-EVs transfected with regent control, or MCPs-EVs transfected with miR-148a-3p inhibitor. The function of miR-148a-3p in MCPs-EVs was evaluated by tube formation assay, migration assay, TUNEL assay, intracavernous pressure, immunofluorescence staining, and western blot experiments. Results: We extracted EVs from MCPs and by small RNA sequencing analysis we found that miR-148a-3p is enriched in MCPs-EVs. Exogenous administration of MCPs-EVs can effectively promote mouse cavernous endothelial cell (MCECs) tube formation, migration, proliferation, and reduce MCECs apoptosis under high-glucose conditions. However, these effects are significantly attenuated in miR-148a-3p-depleted MCPs-EVs, which is extracted after inhibiting miR-148a-3p expression in MCPs. Repeated intracavernous injections of MCPs-EVs improves erectile function by inducing cavernous neurovascular regeneration in diabetic mice. Through online bioinformatics databases and luciferase report assays, we predict Pyruvate dehydrogenase kinase-4 (PDK4) is a potential target gene of miR-148a-3p. Conclusions: Our findings provide new and reliable evidence that miR-148a-3p in MCPs-EVs significantly enhances cavernous neurovascular regeneration by inhibiting PDK4 in diabetic mice.

2023-12-19 | GSE195533 | GEO

Searching targets for miR-32 and miR-148a

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2012-03-29 | E-MEXP-2943 | biostudies-arrayexpress

miR-148a controls metabolic programming and survival of mature CD19-negative plasma cells

Project description:Long-lived antibody-secreting plasma cells are essential to establish humoral memory against pathogens. While a plasma cell gene signature has been established, elaborate key regulators remain enigmatic.The plasma cell signature microRNA miR-148a favors in vitro differentiation of plasmablasts by repressing the germinal center transcription factor Bach2 and pro-apoptotic BIM and PTEN. To determine whether miR-148a fine-tunescontrols the in vivo development of B cells into long-lived plasma cells, we established mice with a genomic, conditional and inducible deletion of miR-148a. The analysis of miR-148a-deficient mice revealed reduced serum Ig, decreased numbers of newly formed plasmablasts and a reduced CD19-negative, CD93-positive long-lived plasma cells compartment. RNASeq and metabolic analysis showed an impaired glucose uptake and oxidative phosphorylation-based energy metabolism, altered abundance of homing receptors CXCR3 (increase) and CXCR4 (reduction) in miR-148a-deficient plasma cells. These findings establish the importance of miR-148a as a regulator of the differentiation and maintenance of late CD19-negative mature plasma cells by controlling their metabolism and retention in the bone marrow niche. clearly undermine our model of miR-148a as a regulator of the maintenance of long-lived plasma cells.

2021-05-21 | GSE156002 | GEO

Profiling of miR-148a responsive genes in HeLa cells

Project description:Comparision of HeLa cells transfected with miR-148a mimic or scramble control for 48h

2015-01-13 | E-MTAB-2411 | biostudies-arrayexpress

RNA-Seq analysis of the WEHI-231-derived stable cell lines WEHI-control and WEHI-miR-148a

Project description:miRNAs regulate the expression of its targets genes by promoting mRNA degradation and translational repression. The goal of this study is to perform RNA-Seq in control or miR-148a-expressing WEHI-231 cell lines for the identification of miR-148a target genes. WEHI-control and WEHI-miR-148a cells were stimulated with anti-IgM (2 ug/ml) for 14 h. Total RNA was extracted, enriched for polyA-containing RNAs and submitted to RNA-Seq.

2016-02-22 | E-GEOD-75809 | biostudies-arrayexpress

RNA-seq analysis after overexpression of miR-148a in keratinocytes

Project description:Identification of the trasncriptional changes linked to over expression of miR-148a in kerratinocytes

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RNA-Seq analysis of the WEHI-231-derived stable cell lines WEHI-control and WEHI-miR-148a

2016-02-22 | GSE75809 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of MicroRNA-148a Inhibited Transcriptomes

Project description:Purpose: MicroRNA-148a regulates the differentiation of dendritic cells. The goals of this study are to identify genes and pathways invovled in the regulation. Methods: Monocytes isolated from wild type or microRNA-148a-/- BM were cultured with GM-CSF and IL-4, or not. Cells were collected at day 0 and day 3. Then, the next-generation libraries of mRNA were prepared using VAHTS mRNA-seq v2 Library Prep Kit for Illumina® (Vazyme, Nanjing, China). The Library quality was determined by Bioanalyzer 4200 (Agilent, Santa Clara, CA, USA). Then the mRNA-seq libraries were sequenced in HiSeq ⅹ10 system (Illumina, San Diego, CA, USA) on a 150bp paired-end run. The differentially expressed genes were selected as having more than 0.5 fold difference in their geometrical mean expression between the compared groups and a statistically significant p-value (<0.05) by analysis of DEseq2. The GO analysis on differentially expressed genes was performed with an R package: Clusterprofiler using a p<0.05 to define statistically enriched GO categories. Pathway analysis was used to determine the significant pathway of the differential genes according to Kyoto Encyclopedia of Genes and Genomes Database (http://www.genome.jp/kegg/) and DAVID Bioinformatics Resources 6.8 (https://david.ncifcrf.gov/). Results: Gene ontology analysis showed that obviously changed genes enriched in autoimmune disease related pathways, suggesting miR-148a is important in autoimmune responses. 990 protein-coding genes upregulated in their mRNA abundance in miR-148a-/- monocytes on day 0, and 1036 genes in miR-148a-/- monocytes on day 3. Among them, 136 genes were found upregulation on both day 0 and 3 in miR-148a-/- monocytes.

2019-12-23 | GSE142511 | GEO

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