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HNF4A-induced lncRNA MIR194-2HG derived miR-194 and miR-192 coordinatively inhibit gastric cancer progression by targeting BTF3L4

ABSTRACT: HNF4A-induced lncRNA MIR194-2HG derived miR-194 and miR-192 coordinatively inhibit gastric cancer progression by targeting BTF3L4

PROVIDER: PRJNA984290 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24940976_1.fastq.gz	Fastqsanger.gz
	SRR24940976_2.fastq.gz	Fastqsanger.gz
	SRR24940977_1.fastq.gz	Fastqsanger.gz
	SRR24940977_2.fastq.gz	Fastqsanger.gz
	SRR24940978_1.fastq.gz	Fastqsanger.gz

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HNF4A-induced lncRNA MIR194-2HG derived miR-194 and miR-192 coordinatively inhibit gastric cancer progression by targeting BTF3L4

Project description:LncRNA MIR194-2HG and derived miR-194 and miR-192 were transcriptionally induced by HNF4A. The oncogenic driver BTF3L4 is identified to be a common target gene of miR-194 and miR-192. Our finding highlights that MIR194-2HG inhibits GC progression through activating the expression miR-192 and miR-194 and repressing BTF3L4 expression.

2023-12-31 | GSE235075 | GEO

U937 miR-194-5p (UmiR-194-5p) vs U937 miR-194-5p (UmiR-194-5p) treated with MS275 (SNDX 275;Entinostat)

Project description:Transcriptional profiling of U937 miR-194-5p (UmiR-194-5p) vs U937 miR-194-5p (UmiR-194-5p) treated with MS275 (SNDX 275;Entinostat) for 24 h at 5uM concetration

2017-05-22 | GSE73647 | GEO

U937 miR-194-5p (UmiR-194-5p) vs U937 miR-194-5p (UmiR-194-5p) treated with SAHA (Vorinostat; suberoylanilide hydroxamic acid)

Project description:Transcriptional profiling of U937 miR-194-5p (UmiR-194-5p) vs U937 miR-194-5p (UmiR-194-5p) treated with SAHA (Vorinostat; suberoylanilide hydroxamic acid) for 24 h at 5uM concetration

2017-05-22 | GSE73648 | GEO

U937 scramble (Usc) vs U937 miR-194-5p (UmiR-194-5p)

Project description:Transcriptional profiling of U937 scramble vs U937 miR-194-5p (UmiR-194-5p)

2017-05-22 | GSE73646 | GEO

Aberrant microRNA expression in radiation-induced rat mammary cancer: the potential role of miR-194 overexpression in cancer cell proliferation.

Project description:Aberrant expression of microRNAs (miRNAs) is frequently associated with a variety of cancers, including breast cancer. We and others have demonstrated that radiation-induced rat mammary cancer exhibits a characteristic gene expression profile and a random increase in aberrant DNA copy number; however, the role of aberrant miRNA expression is unclear. We performed a microarray analysis of frozen samples of eight mammary cancers induced by gamma-irradiation (2 Gy), eight spontaneous mammary cancers, and seven normal mammary samples. We found that a small set of miRNAs was characteristically overexpressed in radiation-induced cancer. Quantitative RT-PCR analysis confirmed that miR-135b, miR-192, miR-194, and miR-211 were significantly upregulated in radiation-induced mammary cancer compared with spontaneous cancer and normal mammary tissue. The expression of miR-192 and miR-194 also was upregulated in human breast cancer cell lines compared with non-cancer cells. Manipulation of the miR-194 expression level using a synthetic inhibiting RNA produced a small but significant suppression of cell proliferation and upregulation in the expression of several genes that are suggested to act as tumor suppressors in MCF-7 and T47D breast cancer cells. Thus, the induction of rat mammary cancer by radiation involves aberrant expression of miRNAs, which may favor cell proliferation.

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Aberrant microRNA expression in radiation-induced rat mammary cancer: the potential role of miR-194 overexpression in cancer cell proliferation.

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Identification of miR-194-5p target genes in gastric cancer

Project description:Increasing studies report that miR-194-5p plays a tumor suppressor role in gastric cancer (GC). Previous studies have revealed that miR-194 inhibited gastric cancer progression through different pathways by affecting the expression level of different target genes. For example, miR-194 have been reported to be able to regulate the expression of FOXM1, NR2F2, BMI1, SDAD1, RBX1, KDM5B, ZEB1 and AKT2 etc. It suggested that miR-194 may play complicated roles in GC. To figure out the mechanism of miR-194' tumor suppressor role in GC, we performed RNA sequencing in two different GC cell lines. Our studies showed that miR-194 tends to regulated target genes by binding on their 3' untranslated regions with either 7-mer-A1 or 7-mer-m8 or 8-mer. Approximately 138 genes were downregulated in both SGC7901 and BGC823 cell lines that transfected with miR-194-5p mimics compared to negative control siRNAs. Most of the downregulated genes have not reported yet.

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Gene expression data from HEK-293T cells transfected with miR-194 mimics

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Gene expression data from HEK-293T cells transfected with miR-194 mimics

Project description:Nuclear factor κB (NF-κB) pathway plays an important role in hepatocellular carcinoma (HCC) progression. miR-194 was previously shown to reduce the induction of NF-κB activity upon addition of tumor necrosis factor α (TNFα). To clarify the molecular mechanism responsible for the effect of miR-194 on NF-κB pathway, mRNA microarray assays were performed to identify the genes that were suppressed by miR-194. HEK-293T cells transfected with miR-194 mimics were cultured for RNA extraction and hybridization on Affymetrix mRNA microarrays. These were compared against the control, which were HEK-293T cells transfected with negative control mimics.

2015-07-01 | E-GEOD-70434 | biostudies-arrayexpress

Coordinated regulation of cell cycle transcripts by p53-inducible microRNAs, miR -192 and -215

Project description:Cell cycle arrest in response to DNA damage is an important anti-tumorigenic mechanism. microRNAs (miRNAs) were shown recently to play key regulatory roles in cell cycle progression. For example, miR-34a is induced in response to p53 activation and mediates G1 arrest by down-regulating multiple cell cycle-related transcripts. Here we show that genotoxic stress promotes the p53-dependent up-regulation of the homologous miRNAs, miR -192 and miR-215. Like miR-34a, activation of miR-192/215 induces cell cycle arrest suggesting that multiple microRNA families operate in the p53 network. Furthermore, we define a downstream gene expression signature for miR-192/215 expression that includes a number of transcripts that regulate G1 and G2 checkpoints. Of these transcripts, 18 transcripts are direct targets of miR-192/215 and the observed cell cycle arrest likely results from a cooperative effect among the modulations of these genes by the miRNAs. Our results demonstrating a role for miR-192/215 in cell proliferation combined with recent observations that these miRNAs are under-expressed in primary cancers support the idea that miR-192 and miR-215 function as tumor-suppressors.

2008-12-07 | GSE13105 | GEO

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