MicroRNA-seq reveals microRNAs under the regulation of miR-125b in NCCIT tumor cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE123156 | GEO | 2018/11/30
REPOSITORIES: GEO
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Project description:To investigate the role and mechanism of miR-125b on NCCIT cells without bias, we analyzed differentially expression RNA profile among miR-125b antagomir-, miR-125b agomir-, and negative control-transfected NCCIT tumor cells by RNA-seq.
2018-11-30 | GSE123113 | GEO
Project description:microRNA-seq reveals microRNAs under the regulation of miR-125b in NCCIT tumor cells
| PRJNA507722 | ENA
Project description:RNA-seq and microRNA-seq reveal RNAs and microRNAs under the regulation of miR-125b in NCCIT tumor cells
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Project description:RNA-seq reveals RNAs under the regulation of miR-125b in NCCIT tumor cells
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Project description:We report here the expression profile of microRNAs in human neuronal differentiation in the neuroblastoma cell line SH-SY5Y. Six microRNAs were significantly upregulated during differentiation induced by all-trans¬-retinoic acid and brain-derived neurotrophic factor. We demonstrated that ectopic expression of either miR-124a or miR-125b increases the percentage of differentiated SH-SY5Y cells with neurite outgrowth. Subsequently, we focused our functional analysis on miR-125b and demonstrated the important role of this miRNA in both spontaneous and induced differentiation of SH-SH5Y cells, based on neurite outgrowth and neuronal marker expression. In human neural progenitor ReNcell VM cells, miR-125b is also upregulated during differentiation and miR-125b ectopic expression significantly promotes neurite outgrowth. To identify the targets of miR-125b regulation, we profiled the global changes in gene expression following miR-125b ectopic expression in SH-SY5Y cells. miR-125b represses 164 genes that contain the seed match sequence of the microRNA and/or predicted to be direct targets of miR-125b by conventional methods. Pathway analysis suggests that a subset of miR-125b-repressed targets antagonize neuronal genes in several neurogenic pathways, thereby mediating the positive effect of miR-125b on neuronal differentiation. We have further validated the binding of miR-125b to the microRNA response elements of ten selected targets. Together, we report here for the first time the important role of miR-125b in human neuronal differentiation. Keywords: mir125-OE/mir-scrambled control comparison & mir125-KD/mir-scrambled control comparsion
2009-02-12 | GSE14787 | GEO
Project description:We demonstrate that miR-125b, a key node in this microRNA regulatory network, is upregulated in gastric cancer (GC) and associated with poor overall survival through an integrated analysis of microRNA and mRNA profiling of GC revealed a mRNA-regulatory network.So we have employed whole genome microarray expression profiling as a discovery platform to compare the transcriptome profiling of human gastric cells (MKN-45) after 48 hours post-transfection of miR-125b mimic (50nM) and mimic control.Pathway analysis shows that the predicted targets of miR-125b are highly involved in apoptosis/program death pathway，and the robust apoptosis genes, BIK and CASP6 are validated as the directed targets of miR-125b.
2021-02-25 | GSE145959 | GEO
Project description:Increasing evidence suggests that microRNAs may play important roles in regulating self-renewal and differentiation in mammalian stem cells (SCs). Here, we explore this issue in skin. We first characterize microRNA expression profiles of skin SCs versus their committed proliferative progenies and identify a microRNA subset associating with “stemness”. Of these, miR-125b is dramatically downregulated in early SC-progeny. We engineer an inducible mice system and show that when miR-125b is sustained in SC-progenies, tissue balance is reversibly skewed towards stemness at the expense of epidermal, oil-gland and HF differentiation. Using gain-and-loss of function in vitro, we further implicate miR-125b as a repressor of SC differentiation. In vivo, transcripts repressed upon miR-125b induction are enriched >700% for predicted miR-125b targets normally downregulated upon SC-lineage commitment. We verify some of these miR-125b targets, and show that Blimp1 and VDR in particular can account for many tissue imbalances we see when miR-125b is deregulated. We used microarrays to compare the global gene expression profile of P4 stage hair follicle ORS cells from DTG (K14-rtTA,TRE-miR-125b) and control littermates.
2011-01-04 | GSE26394 | GEO
Project description:Increasing evidence suggests that microRNAs may play important roles in regulating self-renewal and differentiation in mammalian stem cells (SCs). Here, we explore this issue in skin. We first characterize microRNA expression profiles of skin SCs versus their committed proliferative progenies and identify a microRNA subset associating with “stemness”. Of these, miR-125b is dramatically downregulated in early SC-progeny. We engineer an inducible mice system and show that when miR-125b is sustained in SC-progenies, tissue balance is reversibly skewed towards stemness at the expense of epidermal, oil-gland and HF differentiation. Using gain-and-loss of function in vitro, we further implicate miR-125b as a repressor of SC differentiation. In vivo, transcripts repressed upon miR-125b induction are enriched >700% for predicted miR-125b targets normally downregulated upon SC-lineage commitment. We verify some of these miR-125b targets, and show that Blimp1 and VDR in particular can account for many tissue imbalances we see when miR-125b is deregulated. We used microarrays to compare the global miRNA expression profile of P4 stage hair follicle ORS cells from DTG (K14-rtTA,TRE-miR-125b) and control littermates.
2011-01-04 | GSE26395 | GEO
Project description:MiR-125b possible targets were identified after transfecting a miRNA-mimic (miR-125b) and a scramble miRNA (Negative control) in MCF7 cell line and analyzing gene expression modifications.
2013-12-02 | E-MTAB-1604 | biostudies-arrayexpress
Project description:B-cell acute lymphoblastic leukemia (B-ALL) is often associated with chromosomal translocations leading to the deregulation of proto-oncogenes. MicroRNAs can also be affected by chromosomal alterations and thus contribute to carcinogenesis. The microRNA miR-125b-1 is over-expressed in B-ALL cases with the t(11;14)(q24;q34) translocation, therefore we sought to determine the role of this microRNA in B-cell fate. We used murine pre-BI cells alongside murine and human leukemic B-cell lines to show that miR-125b expression enhances proliferation by targeting Bright/ARID3a, an activator of immunoglobulin heavy-chain transcription. Accordingly, this target gene was down-regulated in B-ALL patients with the t(11;14)(q24;q34) translocation. Repression of Bright/ARID3A blocked differentiation and conferred a survival advantage to Ba/F3 cells under IL3 starvation. In addition, over-expression of miR-125b protected pre-BI and leukemic B-cell lines from apoptosis through blockade of caspase activation via a mechanism that was independent of p53 and BAK1. In summary, miR-125b can act as an oncogene in B-ALL by targeting ARID3a and mediating its repression, thus leading to a blockage in differentiation, increased proliferation and inhibition of apoptosis. To identify specific targets of mir-125b, we overexpressed miR-125b as well as a control miRNA in 70Z/3 and 18-81 pre-B leukaemia cells. Chemically synthesized miRNA duplexes, called pre-miR-125b and miR-Neg, were purchased from Ambion. The cells were transfected with pre-miRNA at a final concentration of 10 nM using Lipofectamin RNAi MAX (Invitrogen) according to the manufacturer’s instructions. The medium was replaced 8 hours after transfection. RNA samples were harvested at 48 hours post-transfection. 2 independent experiments were carried out for a total of 8 samples labeled with Cy3 dye (one color design).
2012-06-20 | E-GEOD-30647 | biostudies-arrayexpress