Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Liver cancer progression through increased miR-221 mediated tumorigenesis

ABSTRACT: Hepatocellular carcinoma (HCC) is the third leading malignancy worldwide. MiR-221 have oncogenic functions and play a seminal role in carcinogenesis regulation including in high risk- human HCC. However, the molecular mechanism and biological functions of miR-221 has not been investigated thoroughly in HCC. In the present work, the role of miR-221 in HCC was evaluated using microarray and miR-221target genes expressions were analyzed in miR-221 inhibitor transfected HCC cell lines HepG2, Huh-7, WRL-68. Finally, we found that 89 upregulated and 52 downregulated genes by miR-221 in HCC cell lines.l

ORGANISM(S): Homo sapiens

PROVIDER: GSE135375 | GEO | 2020/08/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

MicroRNA profiling of human hepatocellular carcinoma samples shows miR-221 overexpression contributes to liver tumorigenesis

Project description:We profiled miRNA expression in tissue samples (104 HCC, 90 adjacent cirrhotic livers, 21 normal livers) as well as in 35 HCC cell lines. A set of 12 miRNAs (including miR-21, miR-221/222, miR-34a, miR-519a, miR-93,miR-96, and let-7c) was linked to disease progression from normal liver through cirrhosis to full-blown HCC. miR-221/222, the most upregulated miRNAs in tumor samples, are shown to target the CDK inhibitor p27 and to enhance cell growth in vitro. Conversely, these activities can be efficiently inhibited by an antagomiR specific for miR-221. In addition, we show, using a mouse model of liver cancer, that miR-221 overexpression stimulates growth of tumorigenic murine hepatic progenitor cells.

2009-12-08 | E-TABM-866 | biostudies-arrayexpress

Gene expression profiling of MCF10A (miR-221/222 vs control)

Project description:Analysis of gene expression of MCF10A to identify the targets of miR-221 and miR-222 Keywords: MCF10, miR-221, miR-222

2011-06-14 | GSE29327 | GEO

Cellular, molecular and proteomic characteristics of early Hepatocellular carcinoma

Project description:Ηepatocellular carcinoma (HCC) accounts for the majority of primary liver cancers. Early de-tection/diagnosis is vital for the prognosis of HCC whereas diagnosis at late stages is associated with very low survival rate. Early diagnosis is based on patient’s 6 month surveillance and use of at least two imaging modalities. The aim of this study was to investigate diagnostic markers for the detection of early HCC based on proteome analysis, microRNAs (miRNAs) and circulat-ing tumor cells (CTCs) in the blood of patients with cirrhosis, early and advanced HCC. We studied 89 patients with HCC of whom 33 had early HCC and 28 cirrhotic patients. CTCs were detected by Real-Time Quantitative Reverse Transcription PCR and immunofluorescence using the markers Epithelial cell adhesion molecule (EPCAM), Vimentin, A Fetoprotein (AFP) and surface major Vault protein (sMVP). Expression of the five most commonly HCC-involved miRNAs (miR-122, miR-200a, miR-200b, miR-221, miR-222) was examined in the serum by qRT-PCR. Finally patient serum was analyzed by whole proteome analysis (LC/MS). Twenty seven out of 53 (51%) patients with advanced HCC had detectable CTCs. Among them, 10/27 (37%) presented evidence of mesenchymal or intermediate stage cells (vimentin and/or sMVP positive). Moreover, 5/17 (29%) patients with early HCC and 6/28 (21%) cirrhotic patients had detectable CTCs. Patients with early and advanced HCC exhibited a significant increase of miR-200b when compared to cirrhotic patients. Our proteome analysis indicated that early HCC patients present a significant upregulation of APOA2, APOC3 proteins when compared to cir-rhotic patients, that when used in combination, cover the 100% of the patients with early HCC. In conclusion, miR-200b, APOA2 and APOC3 proteins are sensitive markers and can be poten-tially useful in combination for the early diagnosis of HCC.

2023-03-11 | PXD033306 | Pride

miR-221 is required for endothelial tip cell behaviors during vascular development

Project description:Through deep sequencing and functional screening in zebrafish, we find that miR-221 is essential for angiogenesis. miR-221 knockdown phenocopied defects associated with loss of the tip cell-expressed Flt4 receptor. Furthermore, miR-221 was required for tip cell proliferation and migration, as well as tip cell potential in mosaic blood vessels. miR-221 knockdown also prevented “hyper-angiogenesis” defects associated with Notch deficiency and miR-221 expression was inhibited by Notch signaling. Finally, miR-221 promoted tip cell behavior through repression of two targets: cyclin-dependent kinase inhibitor 1b (cdkn1b) and phosphoinositide-3-kinase regulatory subunit 1 (pik3r1). These results identify miR-221 as an important regulatory node through which tip cell migration and proliferation are controlled during angiogenesis.

2012-02-28 | GSE35078 | GEO

miR-221 is required for endothelial tip cell behaviors during vascular development

2012-02-28 | E-GEOD-35078 | biostudies-arrayexpress

Gene expression profiling of MCF10A (miR-221/222 vs control)

Project description:Analysis of gene expression of MCF10A to identify the targets of miR-221 and miR-222 Keywords: MCF10, miR-221, miR-222 RNA profiles of human MCF10A cell line

2011-06-14 | E-GEOD-29327 | biostudies-arrayexpress

MiR-221 mediated gene expression in human PCa cells

Project description:MiR-221 overexpression leads to activation of apoptosis, growth arrest and reduced invasivness in PCa cells. Interaction of miR-221 with potential target genes was analyzed by a genome wide expression profiling.. Regulation of selected genes and proteins identified in the gene array analysis was confirmed by Real Time RT-PCR assay (IRF1, IRF2 SOCS3, STAT1), and Western Blotting. In total, 282 genes were upregulated and 64 downregulated based on a more than 2-fold difference to untransfected PC-3 cells. Regulated genes are involved in apoptosis, hemostasis, oxidative stress response, tumorigenesis and inflammation. We confirmed dysregulation of IRF-2 SOCS3, STAT1,IRF9. These results indicate that miR-221 overexpression might lead to activation of the JAK/STAT pathway and downregulation of miR-221 might contribute to tumorigenesis in PCa cells. pre-miR-221 transfected PC-3 cells vs unstimulated control cells - total samples analysed are 4.

2014-03-27 | E-GEOD-45627 | biostudies-arrayexpress

miR-221/222 drive synovial fibroblast expansion and pathogenesis of TNF-mediated arthritis

Project description:MicroRNAs (miRNAs) constitute fine tuners of gene expression and are implicated in a variety of diseases spanning from inflammation to cancer. miRNA expression is deregulated in rheumatoid arthritis (RA), however, their specific role in key arthritogenic cells such as the synovial fibroblast (SF) remains elusive. We have shown in the past that the expression of the miR-221/222 cluster is upregulated in RA SFs. Here, we demonstrate that miR-221/222 activation is downstream of major inflammatory cytokines, such as TNF and IL-1β, which promote miR-221/222 expression independently. miR-221/222 expression in SFs from the huTNFtg mouse model of arthritis correlates with disease progression. Targeted transgenic overexpression of miR-221/222 in SFs of the huTNFtg mouse model led to further expansion of synovial fibroblasts and disease exacerbation. miR-221/222 overexpression altered the transcriptional profile of SFs igniting pathways involved in cell cycle progression and ECM regulation. Validated targets of miR-221/222 included p27 and p57 cell cycle inhibitors, as well as Smarca1 (a chromatin remodeling component). In contrast, complete genetic ablation of miR-221/222 in arthritic mice led to decreased proliferation of fibroblasts, reduced synovial expansion and attenuated disease. scATAC-seq data analysis revealed increased miR-221/222 gene activity in the pathogenic and activated clusters of the intermediate and lining compartment. Taken together, our results establish an SF-specific pathogenic role of the miR-221/222 cluster in arthritis and suggest that its therapeutic targeting in specific subpopulations should inform the design of novel fibroblast-targeted therapies for human disease.

2022-12-16 | GSE210887 | GEO

MiR-221 mediated gene expression in human PCa cells

2014-03-27 | GSE45627 | GEO

Murine bone marrow-derived mast cells (BMMCs) transduced with pAPM lentiviruses overexpressing miR-221 vs control overexpressing miR-221m.

Project description:Bone marrow-derived mast cells were derived from three different female C57Bl/6 mice of similar age. Cells were transduced with pAPM lentiviruses either overexpressing microRNA-221 or a non functional microRNA-221 mutant, termed miR-221m, where four point-mutations were introduced in the seed sequence of miR-221. The samples overexpressing miR-221m were used as references for the corresponding miR-221 overexpressing BMMCs from the same mouse (mouse matched reference). The experiment was performed in order to gain more insights about the molecular mechanisms underlying miR-221 effects in mast cells. Two-condition experiment, BMMC overexpressing miR-221 vs BMMC overexpressing miR-221m. Biological replicates: 3 replicates overexpressing miR-221, 3 control replicates overexpressing miR-221m.

2011-11-23 | E-GEOD-24462 | 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