Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Over-expression of miR-18b is associated with the grade of malignancy of hepatocallular carcinoma

ABSTRACT: Aberrant expression of microRNA (miRNA) is closely associated with carcinogenesis. The malignancy of the hepatocellular carcinoma (HCC) is prescribed in the degree of histological differentiation. Poorly differentiated HCC is generally more malignant prognosis than well differentiated HCC. We analyzed the miRNA expression profiles in 110 HCC (60 moderately differentiated, 30 poorly differentiated, and 20 well differentiated HCC) by using microarray in order to establish the novel biomarker for the degree of histological differentiation and forecasting relapse of HCC. The expression level of 12 miRNAs was significantly different according to the degree of histological differentiation. The expression level of miR-18b in poorly differentiated HCC was significantly higher than that in well differentiated HCC. Based on the target search algorithm and argonaute 2 (Ago2) immunoprecipitation study for target binding assay, miR-18b can control the expression of trinucleotide repeat containing 6B (TNRC6B) as a target. Over expression of miR-18b and down regulation of TNRC6B accelerated the activity of cell proliferation and lost ability of cell adhesion in two hepatoma cell lines. Low expression of miR-18b is significantly decreased the relapse free rate after surgical resection. In conclusion, expression pattern of miR-18b is a marker of an important determinant in the control of cell proliferation and adhesion and also prediction of clinical course. From a clinical point of view, our study emphasizes miR-18b as a diagnostic and prognostic marker for HCC progression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE31164 | GEO | 2013/04/10

SECONDARY ACCESSION(S): PRJNA144801

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

miR-18b overexpression identifies mantle cell lymphoma patients with poor outcome and improves the MIPI-B prognosticator

Project description:Recent studies show that mantle cell lymphoma (MCL) express aberrant miRNA profiles, however, the clinical effect of miRNA expression has not previously been examined and validated in prospective, large, homogenously treated cohorts. We analyzed diagnostic MCL samples from the Nordic MCL2 and MCL3 clinical trials, in which all patients had received Rituximab-high-dose cytarabin alternating with Rituximab-maxiCHOP, followed by BEAM and autologous stem cell support. We performed genome-wide miRNA microarray profiling of 74 diagnostic MCL samples from the MCL2 trial (screening cohort). Differentially expressed miRNAs were re-analyzed by qRT-PCR. Prognostic miRNAs were validated by qRT-PCR in diagnostic MCL samples from 94 patients of the independent MCL3 trial (validation cohort). Three miRNAs (miR-18b, miR-92a, miR-378d) were significantly differentially expressed in patients who died from MCL in both the screening- and the validation cohort. MiR-18b was superior to miR-92a and miR-378d in predicting high risk. Thus, we generated a new MIPI-B-miR prognosticator, combining expression-levels of miR-18b with MIPI-B data. This prognosticator improved identification of high risk patients compared to MIPI-B with regard to cause-specific survival (P=0.015), overall survival (P=0.006) and progression-free survival (P<0.001). Transfection of two MCL cell lines with miR-18b decreased their proliferation rate without inducing apoptosis, suggesting miR-18b may render MCL cells resistant to chemotherapy by decelerating cell proliferation. Thus, we conclude that overexpression of miR-18b identifies patients with poor prognosis in two large prospective MCL cohorts and adds prognostic information to MIPI-B. MiR-18b may reduce the proliferation rate of MCL cells as a mechanism of chemoresistance.

2015-04-01 | GSE66299 | GEO

Histological and clinical effects of Imipramine in the treatment of patients with cancer over-expressing Fascin1.

Project description:Primary objectives: Evaluate the effect of the imipramine treatment on the development of histological manifestations associated with the mesenchymal epithelial transition during the period of time from the analysis of the diagnostic biopsy to the surgical resection intervention. Primary endpoints: Comparison of the histological traits of invasive tumour front of the surgical tumour resection specimen between the intervention group and the placebo group:1. Fascin1 expression in tumour tissue: It will be analysed by immunohistochemistry and the application of Immunoscore.2. Histological manifestations of the epithelial-mesenchymal transition (EMT): Tumour budding, cytoplasmic pseudo-fragments, infiltrating growth pattern and poorly differentiated nests. It will be evaluated by histological analysis.3. Invasive histological manifestations: discontinuous extramural extension, lymphatic, venous and perineural infiltration. It will be evaluated by histological analysis.4. Histological manifestation of the immune response: Peritumoral and intratumour lymphocyte infiltration. It will be evaluated by histological analysis.5. EMT molecular manifestations: FSCN1, SNAIL and SLUG gene expression. It will be evaluated by NGS analysis of the primary tumour.

| 2541275 | ecrin-mdr-crc

Mus musculus

Project description:Transcriptional profile comparing poorly diffentiated HCC nodules to well-differentiated HCC nodules arising in HCC/LECT2-KO mice

| PRJNA388937 | ENA

Growth Differentiation Factor 1-Induced Tumour Plasticity Provides A Therapeutic Window for Immunotherapy in Hepatocellular Carcinoma

Project description:Poorly differentiated hepatocellular carcinoma (HCC) is an aggressive disease with poor prognosis. Here the authors show that GDF1, a member of the TGF-β superfamily, is highly expressed in high-grade poorly differentiated HCC and is associated with tumor plasticity, and that GDF1-induced re-expression of cancer testis antigens could render tumors sensitive to immune checkpoint inhibition.

2021-11-17 | GSE188582 | 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

An integrative analysis of renal miRNA- and mRNA-expression signatures in progressive chronic kidney disease [discovery cohort]

Project description:MicroRNAs (miRNAs) significantly contribute to chronic kidney disease (CKD) progression via regulating mRNA expression and abundance. However, their association with clinical outcome remains poorly understood. We performed large scale miRNA and mRNA expression profiling on cryo-cut renal biopsy sections from n=43 subjects. miRNAs differentiating stable and progressive cases were determined, and putative target mRNAs showing inversely correlated expression profiles were identified and further characterized. We found a downregulation of 7 miRNAs in the progressive phenotype, and an upregulation of 29 target mRNAs which are involved in inflammatory response, cell-cell-interaction, apoptosis, and intracellular signaling. Particularly a diminished expression of miR-206 in progressive disease correlated significantly with the upregulation of the target mRNAs CCL19, CXCL1, IFNAR2, NCK2, PTK2B, PTPRC, RASGRP1, and TNFRSF25, all participating in inflammatory pathways. Progressive cases also showed a decreased expression of miR-532-3p, and an increased expression of target transcripts MAP3K14, TNFRSF10B/TRAIL-R2, TRADD, and TRAF2, all being involved in apoptosis pathways. miR-206, miR-532-3p and all 12 mRNA targets correlated with the degree of histological damage. The identified renal miRNA- and mRNA-profiles, and biological pathways may represent regulatory mechanisms, which are commonly present in various kinds of progressive chronic kidney disease.

2015-12-31 | GSE45980 | GEO

Homo sapiens

Project description:Gene expression profile of poorly differentiated synovial sarcoma

| PRJNA125699 | ENA

Applied Biosystems Human TaqMan Low Density Array (TLDA) in plasma samples from HCC cases and controls

Project description:MicroRNAs (miRNAs) are abundant in the circulation and play a central role in diverse biological processes; they may be useful for early diagnosis of hepatocellular carcinoma (HCC). We conducted a two-phase, case-control study (20 pairs for the discovery set and 49 pairs for the validation set) to test the hypothesis that genome-wide dysregulation of circulating miRNAs differentiate HCC cases from controls. Taqman low density arrays were used to examine genome-wide miRNA expression for the discovery set, and quantitative RT-PCR was used to validate candidate miRNAs for both discovery and validation sets. Sixty-six miRNAs were found to be significantly over-expressed in plasma of HCC cases compared to controls after adjusting for false discovery rate (p<0.05). A volcano plot indicated that 7 miRNAs had greater than 2-fold case-control differences with p<0.01. Four significant miRNAs (miR-150, miR-30c, miR-483-5p and miR-520b) detectable in all samples with varied expression levels were further validated in a validation set. MiR-483-5p was statistically significantly over-expressed in HCC cases compared with controls (3.20 vs. 0.82, p<0.0001). HCC risk factors and clinic-pathological characteristics did not influence miR-483-5p expression. The combination of plasma miR-483-5p level and HCV status can significantly differentiate HCC cases from controls with an AUC of 0.908 (p<0.0001). The sensitivity and specificity were, respectively, 75.5% and 89.8%. These preliminary results suggest the importance of dysregulated circulating miR-483-5p as a potential HCC biomarker. Confirmation of aberrant expression of miR-483-5p in a large prospective HCC study will provide support for its application to HCC detection.

2013-08-21 | GSE50013 | GEO

Microarray analysis of differentiation of human glioblastoma neurospheres

Project description:Brain tumor neurospheres (BTCSs) are cancer cells with neural stem cell-like properties found in the fatal brain tumor glioblastoma multiforme (GBM). These cells account for less than 1% of total tumor cells, are poorly differentiated and are believed to be involved in tumor induction, progression, treatment resistance and relapse. Specific miRNAs play important roles in modulating the proliferation and differentiation of neural stem cells, therefore, we aimed to identify miRNAs controlling differentiation in GBM-BTSCs through high throughput screening miRNA array profiling. We compared the miRNA expression profiles at the neurosphere state and upon 4 and 14days of differentiation by using LIMMA, finding 21 differentially expressed miRNAs : hsa-miR-103, hsa-miR-106a, hsa-miR-106b, hsa-miR-15b, hsa-miR-17, hsa-miR-19a, hsa-miR-20a, hsa-miR-25, hsa-miR-301a and hsa-miR-93 were found up-regulated upon differentiation, while hsa-miR-100, hsa-miR-1259, hsa-miR-21, hsa-miR-22, hsa-miR-221, hsa-miR-222, hsa-miR-23b, hsa-miR-27a, hsa-miR-27b, hsa-miR-29a and hsa-miR-29b were down-regulated. Expression of 11 of the 21 miRNAs was examined by qPCR and 7 of them were validated: hsa-miR-21, hsa-miR-29a, hsa-miR-29b, hsa-miR-221 and hsa-miR-222 increased their expression upon differentiation, while hsa-miR-93 and hsa-miR-106a were inhibited. Functional studies demonstrated that miR-21 over-expression induced the expression of glial and/or neuronal cell markers in the neurospheres, possibly due to SPRY1 targeting by miR-21 in these cells, while miR-221 and miR-222 inhibition at the differentiated state reduced the expression of those differentiation markers. On the other hand, miR-29a and miR-29b targeted MCL1 in the GBM neurospheres and increased apoptotic cell death. Gene expression in differentiated cells relative to neurospheres in four different glioblastoma cultures

2013-03-05 | E-GEOD-44841 | biostudies-arrayexpress

Combined hepatocellular-cholangiocarcinomas exhibit progenitor features and activation of Wnt and TGFbeta signaling pathways

Project description:Primary liver tumours include hepatocellular carcinomas (HCC), cholangiocarcinomas (CC) and a group of rare tumours exhibiting biliary and hepatocytic differentiation called combined hepatocholangiocarcinomas (cHCC-CC). To better define this latter group, we take advantage of a series of these tumours based on their morphological characteristics and we performed transcriptional analysis allowing thereafter global comparison with published data. We show that most cHCC-CCs express progenitor cell traits, are committed to biliary lineage and are mainly associated to the activation of Wnt/beta-catenin and TGFbeta signalling pathways. Wnt/beta-catenin pathway activation in cHCC-CC is evidenced by the expression of both its direct targets such as LEF1 and EPCAM. In addition, extracellular matrix (ECM) genes and ECM-remodelling genes which are upon the control of TGF profibrotic program were found up-regulated in cHCC-CC. Interestingly, we show that CC and most cHCC-CC share characteristics associated to a subtype of poorly differentiated HCC suggesting that these tumours could originate from a stem/progenitor cell. The plasticity of these cells may explain the phenotypical heterogeneity of these tumors with the maintenance of some hepatocellular differentiation features such as albumin expression. Interestingly, this is shared by at least one third of CC, raising the hypothesis of a potential continuum between CC, cHCC-CC and poorly differentiated HCC. Patients serie include 3 intra-hepatic CC, 7 typical HCC and 20 cHCC-CC that was used for microarray hybridisation. All these tumours did not show any mutation of the beta-catenin gene. The degree of hepatic fibrosis of the non-cancerous liver was graded according to the METAVIR classification. Paraffin sections were processed as described previously. Immunohistochemistry was done on standard slides for the series.

2012-03-31 | E-GEOD-35306 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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