Expression profile of EV71-infection-responsive miRNAs
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE75455 | GEO | 2016/01/01
SECONDARY ACCESSION(S): PRJNA304423
REPOSITORIES: GEO
Similar Datasets
Project description:We attempted to identify potential miRNAs that can regulate viral replication by screening host miRNAs in EV71-infected RD cells. To compare the differential expression of miRNAs in EV71-infected cells at different time points, miRNA expression profiles were analyzed using Agilent Human MicroRNA Array chips. At 5 h p.i., the expression levels of most miRNAs in EV71-infected cells were not different from those of mock-infected cells. However, five miRNAs (miR-574-3p, miR-574-5p, miR-181d, miR-197, and miR-939) showed a miRNAs (miR-193a-3p and miR-324-5p) exhibited a increase in expression level in response to EV71 infection at 10 h p.i. RD cells were seeded (2*106 cells) in 10 cm dishes and incubated overnight. The cells were infected with EV71 (strain 2231) on ice at an M.O.I. of 10. After adsorption for 1 h, the virus suspension was replaced with DMEM containing 2% FBS, and the cells were harvested at the indicated times. Total cellular RNA extraction and miRNA microarray analyses were performed using the Agilent Human MicroRNA Array V2 chip, which contains 723 human and 76 viral miRNAs, each with 16 duplicates. Total gene signals were detected and analyzed using the GeneSpring 7.3.1 software and were normalized to the 75th percentile.
2016-07-03 | E-GEOD-75455 | biostudies-arrayexpress
Project description:'MicroRNA (miRNA) is a type of non-coding RNA that regulates the expression of its target genes by interacting with the complementary sequence of the target mRNA molecules. Recent evidence has shown that genotoxic stress induces miRNA expression, but the target genes involved and role in cellular responses remain unclear. We examined the role of miRNA in the cellular response to X-ray irradiation by studying the expression profiles of radio-responsive miRNAs and their target genes in cultured human cell lines. We found that expression of miR-574-3p was induced in the lung cancer cell line A549 by X-ray irradiation. Overexpression of miR-574-3p caused delayed growth in A549 cells. A predicted target site was detected in the 3''-untranslated region of the enhancer of the rudimentary homolog (ERH) gene, and transfected cells showed an interaction between the luciferase reporter containing the target sequences and miR-574-3p. Overexpression of miR-574-3p suppressed ERH protein production and delayed cell growth. This delay was confirmed by knockdown of ERH expression. Our study suggests that miR-574-3p may contribute to the regulation of the cell cycle in response to X-ray irradiation via suppression of ERH protein production. mRNA expression were compared between the A549 cell overexpressing a radio-responsive miRNA and in the A549 cells suppressing the miRNA. Five miRNAs (miR-181d, miR-565, miR-574-3p, miR-629* and miR-766) were examined. Microarray experiments were performed with triplicate for each experiment.'
2014-03-14 | E-GEOD-30131 | biostudies-arrayexpress
Project description:Two miRNA arms from the same precursor, miR-574-5p and miR-574-3p, were reversely expressed and played exact opposite role in gastric cancer progression. miR-574-5p/-3p ratio was also strongly correlated with higher TNM stages and shorter survival of patients. The increase of miR-574-5p/-3p ratio, or the arm-imbalance of miR-574 was due to the dynamic expression of their highly complementary targets in gastric carcinogenesis. The arm imbalance of miR-574 in turn strongly contributed to and further promoted gastric cancer progression. Conclusion: Our findings indicated that targets mediated miR-574 arm-imbalance contributed to gastric cancer progression. Re-modification of the miR-574-targets homeostasis may represent a realistic approach for gastric cancer prevention and therapy. Two miRNA arms from the same precursor, miR-574-5p and miR-574-3p, were reversely expressed and played exact opposite role in gastric cancer progression. miR-574-5p/-3p ratio was also strongly correlated with higher TNM stages and shorter survival of patients. The increase of miR-574-5p/-3p ratio, or the arm-imbalance of miR-574 was due to the dynamic expression of their highly complementary targets in gastric carcinogenesis. The arm imbalance of miR-574 in turn strongly contributed to and further promoted gastric cancer progression. Conclusion: Our findings indicated that targets mediated miR-574 arm-imbalance contributed to gastric cancer progression. Re-modification of the miR-574-targets homeostasis may represent a realistic approach for gastric cancer prevention and therapy. Two miRNA arms from the same precursor, miR-574-5p and miR-574-3p, were reversely expressed and played exact opposite role in gastric cancer progression. miR-574-5p/-3p ratio was also strongly correlated with higher TNM stages and shorter survival of patients. The increase of miR-574-5p/-3p ratio, or the arm-imbalance of miR-574 was due to the dynamic expression of their highly complementary targets in gastric carcinogenesis. The arm imbalance of miR-574 in turn strongly contributed to and further promoted gastric cancer progression. Our findings indicated that targets mediated miR-574 arm-imbalance contributed to gastric cancer progression. Re-modification of the miR-574-targets homeostasis may represent a realistic approach for gastric cancer prevention and therapy.
2019-08-25 | GSE133629 | GEO
Project description:Two miRNA arms from the same precursor, miR-574-5p and miR-574-3p, were reversely expressed and played exact opposite role in gastric cancer progression. miR-574-5p/-3p ratio was also strongly correlated with higher TNM stages and shorter survival of patients. The increase of miR-574-5p/-3p ratio, or the arm-imbalance of miR-574 was due to the dynamic expression of their highly complementary targets in gastric carcinogenesis. The arm imbalance of miR-574 in turn strongly contributed to and further promoted gastric cancer progression. Conclusion: Our findings indicated that targets mediated miR-574 arm-imbalance contributed to gastric cancer progression. Re-modification of the miR-574-targets homeostasis may represent a realistic approach for gastric cancer prevention and therapy.
2019-08-25 | GSE133628 | GEO
Project description:Two miRNA arms from the same precursor, miR-574-5p and miR-574-3p, were reversely expressed and played exact opposite role in gastric cancer progression. miR-574-5p/-3p ratio was also strongly correlated with higher TNM stages and shorter survival of patients. The increase of miR-574-5p/-3p ratio, or the arm-imbalance of miR-574 was due to the dynamic expression of their highly complementary targets in gastric carcinogenesis. The arm imbalance of miR-574 in turn strongly contributed to and further promoted gastric cancer progression. Conclusion: Our findings indicated that targets mediated miR-574 arm-imbalance contributed to gastric cancer progression. Re-modification of the miR-574-targets homeostasis may represent a realistic approach for gastric cancer prevention and therapy.
2019-08-28 | GSE112859 | GEO
Project description:High-throughput profiling of miRNA expression in the livers of vervet monkeys fed a high fructose or chow diet. Analysis of differentially expressed miRNAs revealed miR-148a-3p, miR-181a-5p, miR-342-5p and miR-574-5p may have regulatory roles in coordinating changes in hepatic gene expression in response to a high fructose diet.
2021-12-15 | GSE178269 | GEO
Project description:Microglia were derived from iPSCs and treated with mimics and inhibitors of the miRNAs hsa-miR-150-5p, hsa-miR-193a-3p and hsa-miR-19b-3p. RNA-sequencing was then performed to examine the effects of up- and down-regulation of the respective miRNAs.
| EGAD00001006842 | EGA
Project description:iPSC-derived neurons were treated with mimics and inhibitors of the miRNAs miR-150-5p, hsa-mir-193a-3p and hsa-miR-19b-3p.
RNA-sequencing was then performed to examine the effects of miRNA up-regulation and inhibition.
| EGAD00001006844 | EGA
Project description:We tested the hypothesis that a panel of placental mammal-specific miRNAs and their targets play important to establish receptivity to implantation and their dysregulated expression may be a feature in women with early pregnancy loss. Relative expression levels of miR-340-5p, −542-3p, and −671-5p all increased following treatment of Ishikawa cells with progesterone (10 μg/ml) for 24 hrs (p < 0.05). RNA sequencing of these P4-treated cells identified co-ordinate changes to 6,367 transcripts of which 1713 were predicted targets of miR-340-5p, 670 of miR-542-3p, and 618 of miR-671-5p. Quantitative proteomic analysis of Ishikawa cells transfected with mimic or inhibitor (48 hrs: n=3 biological replicates) for each of the P4-regulated miRNAs was carried out to identify targets of these miRNAs. Excluding off target effects, mir-340-5p mimic altered 1,369 proteins while inhibition changed expression of 376 proteins (p < 0.05) of which, 72 were common to both treatments. A total of 280 proteins were identified between predicted (mirDB) and confirmed (in vitro) targets. In total, 171 proteins predicted to be targets by mirDB were altered in vitro by treatment with miR-340-5p mimic or inhibitor and were also altered by treatment of endometrial epithelial cells with P4. In vitro targets of miR-542-3p identified 1,378 proteins altered by mimic while inhibition altered 975 a core of 200 proteins were changed by both. 100 protein targets were predicted and only 46 proteins were P4 regulated. miR-671-mimic altered 1,252 proteins with inhibition changing 492 proteins of which 97 were common to both, 95 were miDB predicted targets and 46 were also P4-regulated. All miRNAs were detected in endometrial biopsies taken from patients during the luteal phase of their cycle, irrespective of prior or future pregnancy outcomes Expression of mir-340-5p showed an overall increase in patients who had previously suffered a miscarriage and had a subsequent miscarriage, as compared to those who had infertility or previous miscarriage and subsequently went on to have a life birth outcome. The regulation of these miRNAs and their protein targets regulate the function of transport and secretion, and adhesion of the endometrial epithelia required for successful implantation in humans. Dysfunction of these miRNAs (and therefore the targets they regulate) may contribute to endometrial-derived recurrent pregnancy loss in women.
2023-05-10 | PXD036109 | Pride
Project description:We aimed to characterize decoy to the RNA-binding protein CUG-RNA binding protein 1 (CUGBP1 mechanism in A549 lung cancer cells. We identified several new canonical targets of CUGBP1 but those were not regulated by miR-574-5p via the decoy mechanism. This can be explained by the localization of CUGBP1 and miR-574-5p in the nucleus, where CUGBP1 regulates alternative splicing. Next, we analyzed the 3’UTRs of potential targets and found that the decoy-dependent regulation of mPGES-1 splicing is unique. Therefore, we postulate that in A549 cells mPGES-1 is the only protein regulated by the decoy mechanism of CUGBP1 and miR-574-5p which suggests that the decoy mechanism allows the specific regulation of the expression of distinct targets.
2020-03-02 | PXD016803 | Pride