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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

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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. We performed miRNA microarray analysis on mammary carcinomas in Sprague-Dawley rat to identify radiation-specific miRNA expression patterns compared with spontaneous mammary carcinomas and normal mammary tissues.

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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

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.

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

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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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