Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MiR-100-mediated gene expression changes

ABSTRACT: The miR-99 family is one of the evolutionarily most ancient microRNA families, and it plays a critical role in development. There are 3 members of the miR-99 family in humans (miR-99a, miR-99b, miR-100). Recent studies suggested that miR-99 family also regulates various physiological processes in adult tissues, such as wound healing, and a number of diseases processes, including cancer. Here, we aim to identify gene expression changes mediated by miR-99 family in epithelial cells. HaCaT cells and 1386Ln cells were transfected with miR-100 mimic or with negative control mimic (Dharmacon), the total RNA was isolated using miRNeasy Mini kit (Qiagen), and labeled and hydridized to the Affymetrix GeneChip Human Gene 1.0 ST arrays according standard protocol.

ORGANISM(S): Homo sapiens

SUBMITTER: Xiaofeng Zhou

PROVIDER: E-MTAB-1876 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression data after miR-99a transfection in C4-2 prostate cancer cells

Project description:MicroRNAs (miRNAs) have been globally profiled in cancers but there tends to be poor agreement between studies including in the same cancers. Additionally, few putative miRNA targets have been validated. To overcome the lack of reproducibility, we profiled miRNAs by next generation sequencing and locked nucleic acid miRNA microarrays, and we verified concordant changes by quantitative RT-PCR. Notably, miR-125b and the miR-99 family members miR-99a, -99b, -100 were down-regulated in all assays in advanced prostate cancer cell lines relative to the parental cell lines from which they were derived. All four miRNAs were also down-regulated in human prostate tumor tissue compared to normal prostate. Transfection of miR-99a, -99b or -100 inhibited the growth of prostate cancer cells and decreased the expression of prostate-specific antigen (PSA), suggesting potential roles as tumor suppressors in this setting. To identify targets of these miRNAs, we combined computational prediction of potential targets with experimental validation by microarray and polyribosomal loading analysis. Three direct targets of the miR-99 family that were validated in this manner were the chromatin remodeling factors SMARCA5 and SMARCD1 and the growth regulatory kinase mTOR. We determined that PSA is post-transcriptionally regulated by the miR-99 family members at least partially by repression of SMARCA5. Together, our findings suggest key functions and targets of miR-99 family members in prostate cancer suppression and prognosis. C4-2 cells were transfected with miR-99a and harvested after 48hr. si-GL2 was used as control.

2010-12-29 | E-GEOD-26332 | biostudies-arrayexpress

Expression data after miR-99a transfection in C4-2 prostate cancer cells

2010-12-29 | GSE26332 | GEO

miRNA-99 family diverges physiological cardiac hypertrophy to pathological cardiac hypertrophy

Project description:Purpose: The physiological cardiac hypertrophy is an adaptive condition that does not associate with myocyte cell death while pathological hypertrophy is a maladaptive condition associated with myocyte cell death. Alpha-2 macroglobulin (Î±-2M) an acute phase protein induces cardiac hypertrophy via the ERK1,2 and PI3K/Akt signaling. This study is aimed at exploring the miRNome of Î±-2M induced hypertrophied cardiomyocytes and to understand the role of miRNAs in determination of pathological and physiological hypertrophy. Methods: Hypertrophy was induced in H9c2 cardiomyoblasts using alpha-2 macroglobulin. The induction of hypertrophy is confirmed by microscopy and gene expression studies. Subsequently, the total RNA was isolated and small RNA sequencing was executed in Illumina HiSeq 2000. Results: Analysis of small RNA reads revealed the differential expression of a large set of miRNAs during hypertrophy. Among the differentially expressed candidates, miR-99 family (miR-99a, miR-99b and miR-100) showed significant downregulation upon Î±-2M treatment while isoproterenol treatment (pathological hypertrophy) upregulated their expression. The binding site for Egr1 transcription factor was identified in the promoter region of miR-99 family, and interestingly all miRNAs with Egr1 binding site proven by ChIP-Seq were downregulated during physiological hypertrophy Conclusions: The results proved Egr-1 mediated regulation of miR-99 family determines the uniqueness of pathological and physiological hypertrophy. Upregulated miR-99 expression during pathological hypertrophy suggests that it can be a valuable diagnostic marker and potential therapeutic target for cardiac hypertrophy and heart failure. Small RNA profiles of control and hypertrophied cardiomyocyte H9c2 cells were generated by deep sequencing using Illumina HiSeq 2000

2015-11-01 | E-GEOD-73597 | biostudies-arrayexpress

miRNA-99 family diverges physiological cardiac hypertrophy to pathological cardiac hypertrophy

Project description:Purpose: The physiological cardiac hypertrophy is an adaptive condition that does not associate with myocyte cell death while pathological hypertrophy is a maladaptive condition associated with myocyte cell death. Alpha-2 macroglobulin (α-2M) an acute phase protein induces cardiac hypertrophy via the ERK1,2 and PI3K/Akt signaling. This study is aimed at exploring the miRNome of α-2M induced hypertrophied cardiomyocytes and to understand the role of miRNAs in determination of pathological and physiological hypertrophy. Methods: Hypertrophy was induced in H9c2 cardiomyoblasts using alpha-2 macroglobulin. The induction of hypertrophy is confirmed by microscopy and gene expression studies. Subsequently, the total RNA was isolated and small RNA sequencing was executed in Illumina HiSeq 2000. Results: Analysis of small RNA reads revealed the differential expression of a large set of miRNAs during hypertrophy. Among the differentially expressed candidates, miR-99 family (miR-99a, miR-99b and miR-100) showed significant downregulation upon α-2M treatment while isoproterenol treatment (pathological hypertrophy) upregulated their expression. The binding site for Egr1 transcription factor was identified in the promoter region of miR-99 family, and interestingly all miRNAs with Egr1 binding site proven by ChIP-Seq were downregulated during physiological hypertrophy Conclusions: The results proved Egr-1 mediated regulation of miR-99 family determines the uniqueness of pathological and physiological hypertrophy. Upregulated miR-99 expression during pathological hypertrophy suggests that it can be a valuable diagnostic marker and potential therapeutic target for cardiac hypertrophy and heart failure.

2015-11-01 | GSE73597 | GEO

Expression data from ETV6-RUNX1-positive Reh leukemic cells after overexpression of miR-125b, miR-100 and miR-99a levels in different combinations

2013-06-27 | GSE46362 | GEO

Effect of miR-99b-5p on global gene expression in PC3 cells

Project description:We analyzed the effect of negative control mimic and miR-99b-5p mimic on global gene expression in PC3 cells

2021-12-30 | E-MTAB-10350 | biostudies-arrayexpress

Expression data from ETV6-RUNX1-positive Reh leukemic cells after overexpression of miR-125b, miR-100 and miR-99a levels in different combinations

Project description:Combined overexpression of miR-125b with miR-99a and/or miR-100 induced VCR resistance in ETV6-RUNX1-positive leukemic cells Reh. We used microarrays to detail the global changes in gene expression of Reh cells upon enforced expression of miR-125 per se compared with combination of overexpression of miR-125b, miR-100 and/or miR-99a MiR-99a and/or miR-100 were transiently overexpressed in stable miR-125b-expressing and stable scrambled miR-control-expressing Reh cells. Cellular resistance to VCR was determined by MTT assay after incubating the cells with 9 ng/mL VCR for 3 days. Changes in the gene expression pattern of Reh cells induced by miRNAs overexpression were measured using Affymetrix Arrays.

2013-06-27 | E-GEOD-46362 | biostudies-arrayexpress

microRNA array of SH-SY5Y cells

Project description:This experiment captures expression over 60,000 well-annotated RefSeq human transcripts over RNA samples from SH-SY5Y neuroblastoma cells transfected with human and non-human primate microRNA mimic variants of miR-299-3p, miR-503-3p, miR-508-3p and miR-541-3p, as well as a RNA duplex negative control (C2 mimic, Dharmacon).

2016-04-03 | E-MTAB-3617 | biostudies-arrayexpress

Comparative profiling of mRNA expression in human mesenchymal stem cells derived from adult adipose and lipoma tissues

Project description:Human mesenchymal stem cells (MSCs) have been isolated from adult adipose tissues, and were shown to have ability to differentiate into multiple mesodermal lineages as well as non-mesodermal lineages. MSC had also been isolated from lipoma, and the lipoma-derived MSCs (LM6) showed very similar stem cell characteristics to adipose-derived MSCs (AM3). However, LM6 cells exhibited a higher cumulative population doubling levels as compared with AM3 cells. The expression profiles of both mRNAs and microRNAs (miRNAs) from AM3 and LM6 cells were compared to find considerable similarities except that miRNAs miR-99a and miR-152 were abundantly expressed in AM3, but absent in LM6 cells. The abundantly differentially expressed genes HAS2, VNN1, SLC16A6 and COL11A1 in LM6 cells were shown to be targets of miRNAs miR-99a and/or miR-152. Several additional genes were also found to be targets of miRNAs miR-99a and miR-152, as well as let-7g, let-7i, miR-199a, mir-134 and miR-374. The highly up-regulated expression of miRNA target genes such as SLC16A6, COL11A1 and TRHDE, as well as several other genes such as sushi domain containing 2, keratin associated proteins and tumor necrosis factor family, may explain the higher proliferation potential in LM6 cells compared with AM3 cells. Keywords: genetic modification The expression profiles of both mRNAs and miRNAs from the same RNA samples of AM3 and LM6 cells were determined and compared in order to understand the genetic bases for their similarities and differences.

2009-09-08 | E-GEOD-12843 | biostudies-arrayexpress

miR-99a/100~125b tricistrons regulate hematopoietic stem and progenitor cell homeostasis by shifting the balance between TGFM-NM-2 and Wnt signaling

Project description:Although regulation of stem cell homeostasis by miRNAs is well studied, it is unclear how individual miRNAs, genomically encoded within an organized polycistron, can interact to induce an integrated phenotype. miR-99a/100, let-7 and miR-125b paralogues are encoded in two tricistrons on human chromosome 11 and 21. They are highly expressed in hematopoietic stem cells (HSCs) and acute megakaryoblastic leukemia (AMKL), an aggressive form of leukemia with poor prognosis. Integrative analysis of global gene expression profiling, miRNA target prediction and pathway architecture revealed that miR-99a/100, let-7 and miR-125b functionally converge at the combinatorial block of the TGFM-NM-2 pathway by targeting four receptor subunits and two SMAD signaling transducers. In addition, downregulation of tumor suppressor genes APC/APC2 stabilizes active M-NM-2-Catenin and enhances Wnt signaling. By switching the balance between Wnt and TGFM-NM-2 signaling the concerted action of these tricistronic miRNAs promoted sustained expansion of murine and human HSCs in vitro or in vivo, while favoring megakaryocytic differentiation. We lentivirally transduced cord blood CD34+-hematopoietic stem and progenitor cells (CB-HSPCs) to ectopically express miR-125b-2, miR-99a, let-7c or miR-99a~125b-2 and cultured them in megakaryocytic differentiation medium for 7 days.

2014-03-28 | E-GEOD-56335 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data