Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The miR-28-5p targetome discovery identified SREBF2 as one of the mediators of the miR-28-5p tumor suppressor activity in prostate cancer cells

ABSTRACT: The miR-28-5p targetome discovery identified SREBF2 as one of the mediators of the miR-28-5p tumor suppressor activity in prostate cancer cells

PROVIDER: PRJNA600986 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10881968.fastq.gz	Fastqsanger.gz
	SRR10881969.fastq.gz	Fastqsanger.gz
	SRR10881970.fastq.gz	Fastqsanger.gz
	SRR10881971.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

The miR-28-5p targetome discovery identified SREBF2 as one of the mediators of the miR-28-5p tumor suppressor activity in prostate cancer cells

Project description:miR-28-5p is downregulated in some tumor tissues in which it has been demonstrated to have a tumor suppressor (TS) activity. Here, we demonstrate that miR-28-5p acts as a TS in prostate cancer (PCa) cells affecting cell proliferation/survival as well as migration and invasion. Using the miRNA pull out assay and next generation sequencing we collected the complete repertoire of miR-28-5p targets obtaining a data set (miR-28-5p targetome) of 191 mRNAs. Filtering the targetome with TargetScan 7, PITA and RNA22 we found that the 61% of the transcripts had miR-28-5p binding sites. To assign a functional value to the captured transcripts, we grouped the miR-28-5p targets into gene families with annotated function and showed that six transcripts belong to the transcription factor category. Among them we selected SREBF2, a gene with increasing importance in PCa. We validated miR-28-5p/SREBF2 interaction demonstrating that SREBF2 inhibition affects almost all the tumor processes affected by the miR-28-5p re-expression, suggesting that SREBF2 is an important mediator of miR-28-5p TS activity. Our findings support the identification of the targetome of cancer-related miRNAs as a tool to discover genes and pathways fundamental for tumor development and potential new targets for anti-tumor therapy.

2020-02-06 | GSE143589 | GEO

The miR-28-5p Targetome Discovery Identified SREBF2 as One of the Mediators of the miR-28-5p Tumor Suppressor Activity in Prostate Cancer Cells.

Project description:miR-28-5p is downregulated in some tumor tissues in which it has been demonstrated to have tumor suppressor (TS) activity. Here, we demonstrate that miR-28-5p acts as a TS in prostate cancer (PCa) cells affecting cell proliferation/survival, as well as migration and invasion. Using the miRNA pull out assay and next generation sequencing, we collected the complete repertoire of miR-28-5p targets, obtaining a data set (miR-28-5p targetome) of 191 mRNAs. Filtering the targetome with TargetScan 7, PITA and RNA22, we found that 61% of the transcripts had miR-28-5p binding sites. To assign a functional value to the captured transcripts, we grouped the miR-28-5p targets into gene families with annotated function and showed that six transcripts belong to the transcription factor category. Among them we selected SREBF2, a gene with an important role in PCa. We validated miR-28-5p/SREBF2 interaction, demonstrating that SREBF2 inhibition affects almost all the tumor processes altered by miR-28-5p re-expression, suggesting that SREBF2 is an important mediator of miR-28-5p TS activity. Our findings support the identification of the targetome of cancer-related miRNAs as a tool to discover genes and pathways fundamental for tumor development, and potential new targets for anti-tumor therapy.

| S-EPMC7072282 | biostudies-literature

PETACC-8 miR-31-3p and miR-31-5p Ancillary Study

Project description:This is a prospective-retrospective study to determine if the expression of the miRNA’s miR-31-3p and miR-31-5p are prognostic of patient outcomes or predictive of the benefit from anti-EGFR therapy in stage III Colon Cancer. The present study will utilize FFPE tumor samples collected from patients enrolled in the PETACC-8 study conducted by the Fédération Francophone de Cancérologie Digestive (FFCD). This phase 3 clinical trial prospectively randomized fully resected stage III colon cancer patients to receive adjuvant treatment with either FOLFOX-4 plus cetuximab or FLOFOX-4 alone.

| 2260465 | ecrin-mdr-crc

miR-eCLIP of MCF10A cells following treatment with MIR-28 family microRNA mimics

Project description:MIR-28 sibling microRNA mimics (hsa-miR-28-5p or hsa-miR-708-5p) were analyzed by the miR-eCLIP protocol established in Manakov et al. 2022, to determine direct binding targets of these microRNAs in human MCF10A breast epithelial cells.

2024-02-08 | GSE242755 | GEO

miR-1307-5p counteracts breast cancer angiogenesis and metastasis

Project description:MiRNAs have been shown to alter both protein expression and secretion in different cellular contexts. By combining in vitro, in vivo and in silico techniques, we demonstrated that overexpression of pre-miR-1307 reduced the ability of breast cancer cells to induce endothelial cell sprouting and angiogenesis. However, the molecular mechanism behind this and the effect of the individual mature miRNAs derived from pre-miR-1307 on protein secretion and is largely unknown. Here, we overexpressed miR-1307-3p|0, -3p|1 and 5p|0 in MDA-MB-231 breast cancer cells and assessed the impact of miRNA overexpression on protein secretion by Mass Spectrometry. Unsupervised hierarchical clustering revealed a distinct phenotype induced by overexpression of miR-1307-5p|0 compared to the controls and to the 5’isomiRs derived from the 3p-arm. Together, our results suggest different impacts of miR-1307-3p and miR-1307-5p on protein secretion which is in line with our in vitro observation that miR-1307-5p, but not the isomiRs derived from the 3p-arm reduce endothelial cell sprouting in vitro. Hence these data support the hypothesis that miR-1307-5p is at least partly responsible for impaired vasculature in tumors overexpressing pre-miR-1307.

2024-12-11 | PXD041087 | Pride

RNAseq of human tissue culture cells following treatment with MIR-28 family microRNA mimics

Project description:The objectives of this study were to investigate the differential RNAseq profiles of nearly-normal human cell lines treated with MIR-28 family microRNA mimics (hsa-miR-28-5p or hsa-miR-708-5p), compared to negative control.

2024-02-08 | GSE242754 | GEO

RNA-seq profiles of rat cardiomyocytes overexpressing hsa-miR-106b-5p, hsa-miR-93-5p, hsa-miR-25-3p or cel-miR-67

Project description:Myocardial regeneration is restricted to early postnatal life, when mammalian cardiomyocytes still retain the ability to proliferate. The molecular cues that induce cell cycle arrest of neonatal cardiomyocytes towards terminally differentiated adult heart muscle cells remain obscure. We report that the miR-106b~25cluster is higher expressed in the early postnatal myocardium and decreases in expression towards adulthood, especially under conditions of overload, and orchestrates the transition of cardiomyocyte hyperplasia towards cell cycle arrest and hypertrophy by virtue of its targetome. To identify the relevant targets of individual miRNAs in the miR-106b~15 cluster and elucidate the molecular mechanisms underlying the proliferative effects of this microRNA cluster, we assessed the global transcriptomic changes by deep-sequencing total neonatal mouse cardiomyocyte RNA after exogeneous transfection with hsa-miR-106b-5p, hsa-miR-93-5p, hsa-miR-25-3p and compared the transcriptomic profiles to cardiomyocytes transfected with cel-miR-67, a control miRNA.

2021-06-25 | GSE178867 | GEO

Label free proteomic analysis of CAL62/miR-331-5p cells

Project description:The ectopic expression of miR-331-5p suppresses TC cell (CAL62 and TPC-1) malignant behavior was demonstrate

2024-05-24 | PXD039884 | Pride

miR-93-5p is a bona fide Oncodriver Targeting both Classical and Epigenetic Tumor Suppressive Pathways in Liver Cancer

Project description:Purpose: The goals of this study are to compare the transcriptome profiling among LEPC-Control, LEPC-Biotin-miR-93-5p and LEPC-Biotin-miR-93-5p-Muttion group to elevate the enrichment mRNA by Biotin-miR-93-5p in LEPC cells. Methods: LEPC-Control, LEPC-miR-93-5p and LEPC-miR-93-5p-MDX cells mRNA profiles were generated by deep sequencing, in triplicate, using Illumina Hiseq2500/Miseq. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results: we set the increase by ≥ 4 fold and transcripts at an FPKM ≥1 in LEPC cells as significance. By stepwise analysis, we identifies 615 high confident miR-93-5p-targted mature mRNA that is selectively enriched by biotin-miR-93-5p, but not biotin-miR-93-5p mutant, the miR-93-5p targetome we identified by HITS-CLSBP has 97.4% overlap with online predicted miR-93-5p mRNA targets. Conclusions: Overexpression of miR-93-5p instigates the malignant transformation of LEPC by regulating multiple cancer-related pathways.

2019-01-12 | GSE93553 | GEO

Microarray of K562 cell line after overexpression of miR-15a-5p or miR-21-5p.

Project description:The aim was to look for target genes of miR-15a-5p or miR-21-5p.

2021-02-11 | E-MTAB-8776 | biostudies-arrayexpress