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Transcriptomic-based identification of miR-125a novel targets in human hepatocarcinoma cells

ABSTRACT: Transcriptomic-based identification of miR-125a novel targets in human hepatocarcinoma cells

PROVIDER: PRJEB83841 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR14099450_1.fastq.gz	Fastqsanger.gz
	ERR14099450_2.fastq.gz	Fastqsanger.gz
	ERR14099451_1.fastq.gz	Fastqsanger.gz
	ERR14099451_2.fastq.gz	Fastqsanger.gz
	ERR14099452_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Transcriptomic-based identification of miR-125a novel targets in human hepatocarcinoma cells

Project description:The experimental work unveils novel targets of hsa-miR-125a-5p relevant in hepatocellular carcinoma (HCC). In particular, a genome-wide perspective of the whole miR-125a targetome has been achieved. First, two different HCC cell lines were subjected to a miRNA boosting by mimic transfections, resulting in many de-regulated genes, as observed by a transcriptomic approach. Then, the merging of down-regulated genes with results from bioinformatic predictive tools yielded a number of miR-125a direct targets candidates. Finally, those potential targets were further experimentally validated. This study could pave the way to piece together the RNA regulatory networks governed by miR-125a impacting on hepatocarcinogenesis and be exploited in the future for identifying novel biomarkers and therapeutic targets in HCC.

2025-01-27 | E-MTAB-14731 | biostudies-arrayexpress

Transcriptomic-Based Identification of miR-125a Novel Targets in Human Hepatocarcinoma Cells.

Project description:Hepatocellular carcinoma (HCC) is among the most aggressive and lethal human tumors. Many functional studies have demonstrated the role of non-coding RNAs (ncRNA), particularly microRNAs (miRNA), in the regulation of hepatocarcinogenesis driving pathways. MiR-125a-5p (miR-125a) has been consistently reported as an oncosuppressive miRNA, as demonstrated in vivo and in vitro. However, its HCC relevant targets and molecular mechanisms are still largely unknown. Here, a genome-wide perspective of the whole miR-125a targetome has been achieved. In particular, two different HCC cell lines were subjected to a miRNA boosting by mimic transfections, and consequently many genes were de-regulated, as observed by a transcriptomic approach. The merging of down-regulated genes with results from bioinformatic predictive tools yielded a number of candidate direct targets that were further experimentally validated by luciferase-based reporter assays. Different novel targets were found, in particular ARID3A, CCNJ, LIPA, NR6A1, and NUP210, oncogenes in various tumors and here also related to HCC through miR-125a regulation. The RNA interactions investigated in this work could pave the way to piece together the RNA regulatory networks governed by the miRNA impacting on hepatocarcinogenesis, and be exploited in the future for identifying novel biomarkers and therapeutic targets in HCC.

| S-EPMC11763984 | biostudies-literature

Expression profiles of HSPCs overexpressing microRNA cluster 99b/let-7e/125a, miR-125a, miR-155 and empty vector.

Project description:Hematopoietic stem/progenitor cell (HSPC) traits differ between genetically distinct mouse strains. For example, DBA/2 mice have a higher HSPC frequency compared to C57BL/6 mice. We performed a genetic screen for microRNAs that are differentially expressed between LSK, LS−K+, erythroid and myeloid cells isolated from C57BL/6 and DBA/2 mice. This analysis identified 131 microRNAs that were differentially expressed between cell types and 15 that were differentially expressed between mouse strains. Of special interest was an evolutionary conserved miR-cluster located on chromosome 17 consisting of miR-99b, let-7e and miR-125a. All cluster members were most highly expressed in LSKs and down-regulated upon differentiation. In addition, these microRNAs were higher expressed in DBA/2 cells compared to C57BL/6 cells, and thus correlated with HSPC frequency. To functionally characterize these microRNAs, we overexpressed the entire miR-cluster 99b/let-7e/125a and miR-125a alone in BM cells from C57BL/6 mice. Overexpression of the miR-cluster or miR-125a dramatically increased day-35 CAFC activity and caused severe hematopoietic phenotypes upon transplantation. We showed that a single member of the miR-cluster, namely miR-125a, is responsible for the majority of the observed miR-cluster overexpression effects. Finally, we performed genome-wide gene expression arrays and identified candidate target genes through which miR-125a may modulate HSPC fate.

2011-12-15 | GSE33689 | GEO

Gene expression analysis after miR-125a-3p over-expression in oligodendrocyte precursor cells (OPCs)

Project description:MiR-125a-3p over-expression in OPCs impairs their differentiation into fully mature oligodendrocytes. We performed a whole microarray profiling to identify new miR-125a-3p direct targets and altered signaling pathways responsible for its the detrimental effect on oligodendrocyte maturation.

2021-01-21 | GSE143876 | GEO

Expression profiles of HSPCs overexpressing microRNA cluster 99b/let-7e/125a, miR-125a, miR-155 and empty vector.

2011-12-15 | E-GEOD-33689 | biostudies-arrayexpress

CodeLink Mouse Whole Genome Bioarray data from hematopoietic stem cells (HSCs) of miR-125a (+/+) wild-type and miR-125a knockout mice with myeloproliferative disorder (MPD)

2015-12-31 | GSE69621 | GEO

CodeLink™ Mouse Whole Genome Bioarray data from hematopoietic stem cells (HSCs) of miR-125a (+/+) wild-type mice and miR-125a (+/-) heterozygous mice with myeloproliferative disorder

2015-06-30 | GSE65648 | GEO

CodeLink Mouse Whole Genome Bioarray data from hematopoietic stem cells (HSCs) of miR-125a (+/+) wild-type and miR-125a knockout mice with myeloproliferative disorder (MPD)

Project description:miR-125a knockout mice develop myeloproliferative disorder (MPD). To investigate the molecular mechanisms of MPD induced by the loss of miR-125a, gene expression profiling on hematopoietic stem cells of miR-125a (+/+), (+/-) MPD, and (-/-) MPD mice was performed by using CodeLinkTM Whole Genome DNA array analysis. CodeLink Mouse Whole Genome Bioarrays were performed according to the manufacturerâs instruction on total RNA extracted from hematopoietic stem cells of miR-125a (+/+) wild-type mouse, miR-125a (+/-) heterozygous mouse with MPD, and miR-125a (-/-) homozygous mouse with MPD. One replicate per array.

2015-12-31 | E-GEOD-69621 | biostudies-arrayexpress

miR-125a Confers Multi-Lineage Long-Term Repopulating Stem Cell Activity to Murine and Human Hematopoietic Progenitors

Project description:Umbilical cord blood (CB) is a non-invasive, convenient and broadly used source of hematopoietic stem cells (HSCs) for allogeneic stem cell transplantation. However, limiting numbers of HSCs remain a major constraint for its clinical application. One feasible option would be to expand HSCs to improve therapeutic outcome, however available protocols and the molecular mechanisms governing the self-renewal of HSC are unclear. Here we show that ectopic expression of a single miRNA, miR-125a, in purified murine and human multipotent progenitors (MPP) resulted in increased self-renewal and robust long-term multi-lineage repopulation in transplanted recipient mice. Using quantitative proteomics and Western blot analysis, we identified a restricted set of miR-125a targets which revealed the involvement of the MAP kinase signaling pathway in conferring long-term repopulating capacity to multipotent progenitors in human and mice. Our findings offer the innovative potential to use MPP with enhanced self-renewal activity to augment limited sources of HSC to improve clinical protocols.

2017-01-11 | PXD003931 | Pride

CodeLink™ Mouse Whole Genome Bioarray data from hematopoietic stem cells (HSCs) of miR-125a (+/+) wild-type mice and miR-125a (+/-) heterozygous mice with myeloproliferative disorder

Project description:miR-125a knockout mice develop myeloproliferave disorder (MPD). To investigate the molecular mechanisms of MPD induced by the loss of miR-125a, gene expression profiling on hematopoietic stem cells of miR-125a (+/+) and (+/-) MPD mice was performed using CodeLink Whole Genome DNA array analysis. Codelink Mouse Whole Genome Bioarrays were performed according to the manufacturer’s instruction on total RNA extracted from hematopoietic stem cells of miR-125a (+/+) wild-type mice and miR-125a (+/-) heterozygous mice with MPD. One replicate per array.

2015-06-30 | E-GEOD-65648 | biostudies-arrayexpress

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