Hsa-miR-375/RASD1 signaling predicts local control in early breast cancer
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PROVIDER: PRJNA659262 | ENA |
REPOSITORIES: ENA
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Project description:Hsa-miR-375/RASD1 signaling predicts local control in early breast cancer
| PRJNA659262 | ENA
Project description:Cervical cancer results from the accumulation of (epi)genetic aberrations following persistent infection with high-risk human papillomavirus (HPV). In order to define genetic aberrations associated with cervical carcinogenesis, chromosomal profiles of high-grade cervical intraepithelial neoplasia (CIN) were generated. Common aberrations usually encompass large genomic regions and contain numerous genes, hampering identification of actual driver genes. Consequently, direct evidence of chromosomal alterations actively contributing to cervical carcinogenesis has been lacking so far. By analyzing 60 high-grade CIN with high resolution arrayCGH we identified focal chromosomal aberrations that each harbour only one or a few genes. In total 74 focal aberrations were identified encoding 305 genes. Analysis of genes located within these focal aberrations, using two independent expression microarray datasets, revealed concurrent altered expression in high-grade CIN and/or cervical carcinomas compared to normal cervical samples for 8 genes: ATP13A3, HES1, OPA1, HRASLS, EYA2, ZMYND8, APOBEC2 and NCR2. Gene silencing of EYA2, located within a focal gain at 20q13, significantly reduced viability and migratory capacity of HPV16-transformed keratinocytes. Interestingly, for hsa-miR-375, located within the most frequently identified focal loss at 2q35, a direct correlation between a (focal) loss and significantly reduced expression was found. Down-regulation of hsa-miR-375 expression during cervical carcinogenesis was confirmed in a second independent series of cervical tissues. Moreover, ectopic expression of hsa-miR-375 in 2 cervical carcinoma cell lines reduced cellular viability. In conclusion, our data provide a proof of concept that chromosomal aberrations are actively contributing to HPV-induced carcinogenesis and identify EYA2 and hsa-mir-375 as oncogene and tumor suppressor gene, respectively. DNA from microdissected tissues: 60 samples total. 11 high-grade CIN, <5yr preceding hrHPV infection, 43 high-grade CIN >5yr preceding hrHPV infection, 6 CIN3 adjacent to SCC
2012-12-31 | E-GEOD-34575 | biostudies-arrayexpress
Project description:Cervical cancer results from the accumulation of (epi)genetic aberrations following persistent infection with high-risk human papillomavirus (HPV). In order to define genetic aberrations associated with cervical carcinogenesis, chromosomal profiles of high-grade cervical intraepithelial neoplasia (CIN) were generated. Common aberrations usually encompass large genomic regions and contain numerous genes, hampering identification of actual driver genes. Consequently, direct evidence of chromosomal alterations actively contributing to cervical carcinogenesis has been lacking so far. By analyzing 60 high-grade CIN with high resolution arrayCGH we identified focal chromosomal aberrations that each harbour only one or a few genes. In total 74 focal aberrations were identified encoding 305 genes. Analysis of genes located within these focal aberrations, using two independent expression microarray datasets, revealed concurrent altered expression in high-grade CIN and/or cervical carcinomas compared to normal cervical samples for 8 genes: ATP13A3, HES1, OPA1, HRASLS, EYA2, ZMYND8, APOBEC2 and NCR2. Gene silencing of EYA2, located within a focal gain at 20q13, significantly reduced viability and migratory capacity of HPV16-transformed keratinocytes. Interestingly, for hsa-miR-375, located within the most frequently identified focal loss at 2q35, a direct correlation between a (focal) loss and significantly reduced expression was found. Down-regulation of hsa-miR-375 expression during cervical carcinogenesis was confirmed in a second independent series of cervical tissues. Moreover, ectopic expression of hsa-miR-375 in 2 cervical carcinoma cell lines reduced cellular viability. In conclusion, our data provide a proof of concept that chromosomal aberrations are actively contributing to HPV-induced carcinogenesis and identify EYA2 and hsa-mir-375 as oncogene and tumor suppressor gene, respectively.
2012-12-31 | GSE34575 | GEO
Project description:The current analysis was a two phase study. The first step of the pilot phase comprised an in-silico search for potential target molecules in five different databases. The second step was a screen for potential targets in 28 patients (14 with local relapse and 14 matched controls) by means of microarray technology. The combined results formed the basis for the validation phase in an independent set of 53 patients performed with droplet digital PCR (ddPCR).
2021-01-01 | GSE156873 | GEO
Project description:We constructed a genome wide target profile of hsa-miR-503, hsa-miR-103, and hsa-miR-494 by sequencing RNA isolated from Ago2 immunoprecipitations and total RNA samples following transfection of the respective miRNA in mature duplex form
2015-02-04 | GSE64615 | GEO
Project description:We report the application of transcriptome sequencing for investigating of the hsa-miR-371a-5p and hsa-miR-518a-3p regulated genes. JAR, JEG-3 and BeWo choriocarcinoma cells were transfected with hsa-miR-371a-5p or hsa-miR-518a-3p inhibitors or control inhibitors. Totally, 237, 132 and 277 genes with > 2 folds change and adjusted P < 0.05 were upregulated in JAR, JEG-3 and BeWo cells respectively after hsa-miR-371a-5p knockdown. Meanwhile, 229, 269 and 191 genes were upregulated in JAR, JEG-3 and BeWo cells respectively after hsa-miR-518a-3p knockdown. The top upregulated genes included many oncogenes or oncogenesis associated ones. Enrichment analysis showed hsa-miR-371a-5p and hsa-miR-518a-3p regulated diverse pathways related to tumorigenesis and metastasis. Our results would be helpful for the searching of early molecular biomarkers and therapeutic targets for gestational trophoblastic neoplasia.
2018-11-01 | GSE106394 | GEO
Project description:We constructed a genome wide target profile of hsa-miR-503, hsa-miR-103, and hsa-miR-494 by sequencing RNA isolated from Ago2 immunoprecipitations and total RNA samples following transfection of the respective miRNA in mature duplex form Examination of mRNA levels in HeLa cells and Ago2 immunoprecipitations from HeLa cells following miR-503, miR-103, or miR-494 mature duplex or control siRNA transfection
2015-02-04 | E-GEOD-64615 | biostudies-arrayexpress
Project description:Specificity of interaction between a microRNA (miRNA) and its targets crucially depends on the seed region located in its 5’-end. It is often implicitly considered that two miRNAs sharing the same biological activity should display similarity beyond the strict six nucleotide region that forms the seed, in order to form specific complexes with the same mRNA targets. We have found that expression of hsa-miR-147b and hsa-miR-210, though triggered by different stimuli (i.e. lipopolysaccharides and hypoxia, respectively), induce very similar cellular effects in term of proliferation, migration and apoptosis. Hsa-miR-147b only shares a “minimal” 6-nucleotides seed sequence with hsa-miR-210, but is identical with hsa-miR-147a over 20 nucleotides, except for one base located in the seed region. Phenotypic changes induced after heterologous expression of miR-147a strikingly differ from those induced by miR-147b or miR-210. In particular, miR-147a behaves as a potent inhibitor of cell proliferation and migration. These data fit well with the gene expression profiles observed for miR-147b and miR-210, which are very similar, and the gene expression profile of miR-147a, which is distinct from the two others. Bioinformatics analysis of all human miRNA sequences indicates multiple cases of miRNAs from distinct families exhibiting the same kind of similarity that would need to be further characterized in terms of putative functional redundancy. Besides, it implies that functional impact of some miRNAs can be masked by robust expression of miRNAs belonging to distinct families. To compare the set of transcripts targeted by hsa-miR-147a, hsa-miR-147b and hsa-miR-210, we overexpressed these miRNAs in human lung adenocarcinoma A549 cells by transfecting them with synthetic pre-miRNAs or a synthetic “negative” pre-miRNA as a control (miR-Neg). RNA samples were harvested at 48 hours post-transfection and 3 independent experiments were carried out. 48 hours post-transfection, 3 independent experiments were performed in dye-swap: hsa-miR-147a versus miR-Neg; hsa-miR-147b versus miR-Neg; hsa-miR-210 versus miR-Neg.
2012-08-20 | E-GEOD-33247 | biostudies-arrayexpress
Project description:We attempted to identify the miR-375-3p target genes using a microarray analysis to evaluate the function and transfection efficiency of miR-375-3p mimic.
2023-08-13 | GSE240389 | GEO
Project description:RNA-seq profiles of rat cardiomyocytes overexpressing hsa-miR-106b-5p, hsa-miR-93-5p, hsa-miR-25-3p or cel-miR-67
| PRJNA741260 | ENA