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The Co-regulated Genes by Ectopic Expression of MiR-371-372-373 Cluster in HepG2 Cells

ABSTRACT: MicroRNAs are important cellular regulators and their dysfunctions are associated with various disease. miR-371/372/373 was found co-regulated in HBV-producing HepG2.2.15 cells when compared to its non-HBV producing maternal HepG2 cells. To obtain a glimpse of the potential influence of the enforced miR-371-372-373 cluster in HepG2 gene expression, a two-color Capitalbio 70-mer oligo microarray platform, which contained 21,329 well-characterized human gene probes, was used to identify the differentially expressed genes between miR-371-372-373-HepG2 and mock-HepG2 in two independent biological replicate.

ORGANISM(S): Homo sapiens

PROVIDER: GSE19981 | GEO | 2012/01/15

SECONDARY ACCESSION(S): PRJNA120137

REPOSITORIES: GEO

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The Co-regulated Genes by Ectopic Expression of MiR-371-372-373 Cluster in HepG2 Cells

Project description:MicroRNAs are important cellular regulators and their dysfunctions are associated with various disease. miR-371/372/373 was found co-regulated in HBV-producing HepG2.2.15 cells when compared to its non-HBV producing maternal HepG2 cells. To obtain a glimpse of the potential influence of the enforced miR-371-372-373 cluster in HepG2 gene expression, a two-color Capitalbio 70-mer oligo microarray platform, which contained 21,329 well-characterized human gene probes, was used to identify the differentially expressed genes between miR-371-372-373-HepG2 and mock-HepG2 in two independent biological replicate. miR-371-372-373-HepG2 vs. mock-HepG2

2012-01-15 | E-GEOD-19981 | biostudies-arrayexpress

Differentially expressed miRNAs between HepG2.2.15 and HepG2 cells

Project description:MiRNAs are important posttranscriptional regulators in various physiological processes and their dysregulations have been found in diseases such as infection, imflammation and cancer. Here we compared the miRNA profilings between HBV-producing HepG2.2.15 and its non-HBV maternal HepG2 cell to find potential miRNAs involving in HBV expression. The result indicated that some of the deregulated miRNAs in HepG2.2.15 have been implicated in viral infection and the processes of the immune regulation. HepG2.2.15 vs. HepG2

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Identification of differentially expressed genes between control and miR-371~373 cluster-overexpressing colorectal cancer cells

Project description:The miR-371~373 cluster is a suspected repressor of colon cancer initiation and progression. To better understand its role in metastasis initiation, we used microarray expression analysis to identify potential target genes of this miRNA cluster Potential target genes were defined as significantly downregulated genes after stable overexpression of the miR-371~373 cluster

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Analysis of micorRNA expression during the HBV acute and chronic infections

Project description:Recent implication of microRNAs (miRNAs) in the intricate cross-talk between the host and the pathogen in viral infections reveals a new layer of mechanism for host-virus interactions. In the present study, we investigated human miRNAs which may be involved in the acute and chronic HBV infections via microarray profiling. We determined the global miRNA expression profiles elicited in the uninfected control model (HepG2), the acute infection model (HepG2 transfected with a 1.3 full-length HBV genome) and the chronic infection model (HepG2.2.15) using CapitalBio corporation’s mammalian miRNA arrays. Three cellular models were used in this study: the human hepatoblastoma cell line HepG2 as a blank control representing the condition without virus infection; HepG2 transfected with a 1.3 full-length HBV genome as an acute infection model; and HepG2.2.15, a well-established cell line derived from HepG2 transfected with a full-length HBV genome and constitutively expressing HBV, as a chronic infection model.

2010-06-16 | E-GEOD-22378 | biostudies-arrayexpress

MiR-192 inhibits nucleotide excision repair by targeting ERCC3 and ERCC4 in HepG2.2.15 cells.

Project description:Deficient DNA repair capacity is associated with genetic lesions accumulation and susceptibility to carcinogenesis. MicroRNAs (miRNAs) are small non-coding RNAs that regulate various cellular pathways including DNA repair. Here we hypothesized that the existence of HBV products may interfere with cellular nucleotide excision repair (NER) through microRNA-mediated gene regulation. We found that NER was impaired in HepG2.2.15 cells, a stable HBV-expressing cell line, compared with its parental cell line HepG2. Altered miRNA expression profile, in particular the significant upregulation of miR-192, was observed in HepG2.2.15 cells. Additionally, ERCC3 and ERCC4, two key factors implicated in NER, were identified as targets of miR-192 and over-expressing miR-192 significantly inhibited cellular NER. These results indicated that persistent HBV infection might trigger NER impairment in part through upregulation of miR-192, which suppressed the levels of ERCC3 and ERCC4. It provides new insight into the effect of chronic HBV infection on NER and genetic instability in cancer. A genome-wide miRNAs microarray was performed to identify differentially expressed miRNAs between HepG2.2.15, a stable HBV-expressing cell line, and its parental cell line HepG2.

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Analysis of micorRNA expression during the HBV acute and chronic infections

2010-06-17 | GSE22378 | GEO

Differentially expressed miRNAs between HepG2.2.15 and HepG2 cells

2011-01-14 | GSE19980 | GEO

Targeting oncogenic microRNAs from the miR-371~373 and miR-302/267 clusters in malignant germ cell tumours causes growth inhibition through cell cycle disruption

Project description:Background. MiR-371~373 and miR-302/367 cluster over-expression occurs in all malignant- GCTs, regardless of age (paediatric/adult), site (gonadal/extragonadal), or subtype [seminoma, yolk sac tumour (YST), embryonal carcinoma (EC)]. Six of eight microRNAs from these clusters contain the seed ‘AAGUGC’, determining mRNA targeting. Here we sought to identify the significance of these observations by targeting these microRNAs functionally. Methods. We targeted miR-371~373 and/or miR-302/367 clusters in malignant-GCT cell lines, using CRISPR-Cas9, gapmer primary miR-302/367 transcripts inhibition, and peptide- nucleic-acid (PNA) or locked-nucleic-acid (LNA)-DNA inhibition targeting miR-302a-d-3p, and undertook relevant functional assays. Results. MiR-302/367 cluster microRNAs made the largest contribution to AAGUGC seed abundance in malignant-GCT cells, regardless of subtype (seminoma/YST/EC). Following unsuccessful use of CRISPR-Cas9, gapmer, and PNA systems, LNA-DNA-based targeting resulted in growth inhibition in seminoma and YST cells. This was associated with de- repression of multiple mRNAs targeted by ‘AAGUGC’ seed-containing microRNAs, with pathway analysis confirming predominant disruption of Rho-GTPase signaling, vesicle organization/transport, and cell-cycle regulation, findings corroborated in clinical samples. Further LNA-DNA inhibitor studies confirmed direct cell-cycle effects, with increase of cells in G0/G1-phase and decrease in S-phase. Conclusion. Targeting of specific miR-371~373 and miR-302/367 microRNAs in malignant- GCTs demonstrated their functional significance, with growth inhibition mediated through cell-cycle disruption.

2024-08-01 | E-MTAB-13323 | biostudies-arrayexpress

Homo sapiens

Project description:The Co-regulated Genes by Ectopic Expression of MiR-371-372-373 Cluster in HepG2 Cells

| PRJNA120137 | ENA

Real-Time qPCR Array of miRNAs in Leishmania-infected THP-1 macrophages

Project description:Leishmania amazonensis is a protozoan that primarily infects macrophages and causes cutaneous leishmaniasis in humans. MicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression at posttranscriptional levels. Previous work demonstrated changes in miRNA profile of host cells favoring parasite survivel. Thus, here we demonstrate that human macrophages upregulate several miRNAs on the initial time points of infection, including the hsa-miR-372, hsa-miR-373, and hsa-miR-520d, which present the same seed. Further functional analysis demonstrated that inhibition of the miR-372 impaired Leishmania survival in THP-1 macrophages and the effect was further enhanced with combinatorial inhibition of the miR-372/373/520d family, pointing to a cooperative mechanism. Our study demonstrated miRNA-dependent modulation of polyamines production, establishing permissive conditions for intracellular parasite survival.Our findings suggest that the miR-372/373/520d family may represent a potential target for the development of new therapeutic strategies against cutaneous leishmaniasis.

2023-09-11 | GSE242513 | GEO

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