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Gene expression profile from single cell level of retinal cells from optic cup of injected Abca4KO mice with miR-181a/b sponge therapeutic

ABSTRACT: We observed a beneficial effect on Abca4KO mice phenotype upon miR-181a/b sponge treatment. Then, we decided to perform single cell analysis to better understand the pathway associated with amelioration observed.

ORGANISM(S): Mus musculus

PROVIDER: GSE278172 | GEO | 2026/07/31

REPOSITORIES: GEO

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Gene expression profile from single cell level of retinal cells from optic cup of injected Abca4KO mice with miR-181a/b sponge therapeutic

Project description:We observed a beneficial effect on Abca4KO mice phenotype upon miR-181a/b sponge treatment. Then, we decided to perform single cell analysis to better understand the pathway associated with amelioration observed. Abca4KO mice were injected with miR-181a/b sponge in one eye and with a control vector in the controlateral. Subretinal injection were performed at 2 months of age and samples collected and analyzed at 4 months post-treatment. In a second experiment Abca4KO and WT mice were analyzed analyzed at 4 months.

2026-02-20 | E-MTAB-15988 | biostudies-arrayexpress

Gene expression profile from single cell level of retinal cells from optic cup of injected Abca4KO mice with miR-181a/b sponge therapeutic

Project description:Gene expression profile from single cell level of retinal cells from optic cup of injected Abca4KO mice with miR-181a/b sponge therapeutic

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Gene expression profile from single cell level of retinal cells from optic cup of injected Abca4KO mice with miR-181a/b sponge therapeutic

Project description:Gene expression profile from single cell level of retinal cells from optic cup of injected Abca4KO mice with miR-181a/b sponge therapeutic

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miR-181a modulates Acute Myeloid Leukemia susceptibility to natural killer cells

Project description:Overexpression of miR-181a in AML blasts: DNA Microarray was performed to compare overall gene expression profiles of KG-1 Anti-miR-CT and U937 Anti-miR-CT cells compared respectively to KG-1 Anti-miR-181a and U937 Anti-miR-181a.

2014-12-30 | E-MTAB-2837 | biostudies-arrayexpress

Comparison of miR-181a transfected K562 cells and mock transfected K562 cells

Project description:This series consists of samples taken from two groups of K562 cells(miR-181a transfected group and control group ) and harvested 48 hours later. We used Agilent human 1A oligo microarray identified the changes in gene expression profile of K562 cells after miR-181a transfection experiment. Further studies aimed to find target mRNA of miR-181a in mammalian cells and its biological function. Keywords = miR-181a Keywords = microarray Keywords = K562 Keywords: microRNA transfection analysis

2005-11-18 | GSE3605 | GEO

Identifying downstream targets of microRNA-181a in chondrosarcoma cells.

Project description:microRNAs are small (22-24 nucleotide), non-coding RNA transcripts that play a role in RNA silencing and post transcriptional regulation of gene expression. They have been implicated to have profound roles in many cancers. The role of microRNAs in chondrosarcoma progression is not well understood. Our lab has identified miR-181a to be up-regulated in chondrosarcoma. miR-181a modulates CXCR4 signaling by targeting RGS-16, leading to increased levels of VEGF and MMP-1, major factors in tumor invasion. In an effort to identify other targets of miR-181a apart from RGS-16, we carried out a gene array to compare gene expression between untreated/control CS-1(chondrosarcoma cell line) cells and CS-1 cells transduced with a lenti virus expression construct with anti-miR-181a sequence.

2018-06-19 | GSE70065 | GEO

Identification of miR-181a target genes in Epithelial Ovarian Cancer

Project description:We have identified a single miRNA, miR-181a, that can modulate TGF-Î² signaling to induce and maintain EMT, and effect further downstream events of tumour cell survival, altered response to chemotherapy, migration, invasion and dissemination in vivo. Our present study provides an understanding of how enhanced expression of miR-181a can confer malignant and invasive traits through the modulation of a canonical signaling pathway and a consequent maintenance of a mesenchymal state. Furthermore, inhibition of miR-181a led to a reversion of EMT and subsequent events through decreased TGF-Î² signaling. Our data confirmed Smad7 as a functional target through which TGF-Î²-mediated EMT occurs; re-expression of Smad7 lacking its 3'UTR was able to rescue miR-181a-mediated phenotypes, deeming Smad7 as a critical mediator of miR-181a-induced EMT. Other recent studies support the crucial role(s) that miRNAs play in mediating EMT and consequent aggressive disease traits. For example, the miR-106b-25 cluster has also been shown to target Smad7 and mediate TGF-Î²-induced EMT downstream to Six1 in breast cancer34. miR-9 directly targets E-cadherin and inhibition of miR-9 had led to an inhibition of metastasis35. Conversely, the miR-200 and -205 family was shown to target transcriptional repressors of E-cadherin, ZEB1 and SIP1, and re-expression of these miRNAs led to a mesenchymal-to-epithelial transition and prevented TGF-Î² -induced EMT36. A2780 ovarian cancer cell lines stably expressing either pBABE (control vector), p181a#1( clone 1 expressing miR-181a) or p181a#2( clone 2 expressing miR-181a)

2013-12-01 | E-GEOD-52077 | biostudies-arrayexpress

Lenalidomide-mediated enhanced translation of C/EBP?-p30 protein upregulates expression of the anti-leukemic microRNA-181a in acute myeloid leukemia - microRNA Data

Project description:Recently, we showed that increased miR-181a expression was associated with improved outcomes in cytogenetically normal acute myeloid leukemia (CN-AML). Interestingly, miR-181a expression was increased in CN-AML patients harboring CEBPA mutations, which are usually biallelic and associate with better prognosis. CEBPA encodes the C/EBP? transcription factor. We demonstrate here that the presence of N-terminal CEBPA mutations and miR-181a expression are linked. Indeed, the truncated C/EBP?-p30 isoform, which is produced from the N-terminal mutant CEBPA gene or from the differential translation of wild-type CEBPA mRNA and is commonly believed to have no transactivation activity, binds to the miR-181a-1 promoter and upregulates the microRNA expression. In xenograft mouse models, ectopic miR-181a expression inhibits tumor growth. This regulatory pathway may explain an increased sensitivity to apoptosis-inducing chemotherapy in subsets of AML patients. Altogether, our data provide a potential explanation for the improved clinical outcomes observed in CEBPA-mutated CN-AML patients.

2012-10-04 | E-MTAB-1320 | biostudies-arrayexpress

Screening and identification of miR-181a-5p in oral squamous cell carcinoma and functional verification in vivo and in vitro

Project description:Background: Oral squamous cell carcinoma (OSCC) is a common malignant tumor associated with poor prognosis. MicroRNAs (miRNAs) play crucial regulatory roles in the cancer development. However, the role of miRNAs in OSCC development and progression is not well understood. Methods: We sought to establish a dynamic Chinese hamster OSCC animal model, construct miRNA differential expression profiles of its occurrence and development, predict its targets, and perform functional analysis and validation in vitro. Results: Using expression and functional analyses, the key candidate miRNA (miR-181a-5p) was selected for further functional research, and the expression of miR-181a-5p in OSCC tissues and cell lines was detected. Subsequently, transfection technology and a nude mouse tumorigenic model were used to explore potential molecular mechanisms. miR-181a-5p was significantly downregulated in human OSCC specimens and cell lines, and decreased miR-181a-5p expression was observed in multiple stages of the Chinese hamster OSCC animal model. Moreover, upregulated miR-181a-5p significantly inhibited OSCC cell proliferation, colony formation, invasion, and migration; blocked the cell cycle; and promoted apoptosis. BCL2 was identified as a target of miR-181a-5p. BCL2 may interact with apoptosis- (BAX), invasion- and migration- (TIMP1, MMP2, and MMP9), and cell cycle-related genes (KI67, E2F1, CYCLIND1, and CDK6) to further regulate biological behavior. Tumor xenograft analysis indicated that tumor growth was significantly inhibited in the high miR-181a-5p expression group. Conclusions: Our findings indicate that miR-181a-5p can be used as a potential biomarker and provide a novel animal model for mechanistic research on oral cancer.

2023-01-10 | GSE222429 | GEO

Identification of miR-181a target genes in Epithelial Ovarian Cancer

Project description:We have identified a single miRNA, miR-181a, that can modulate TGF-β signaling to induce and maintain EMT, and effect further downstream events of tumour cell survival, altered response to chemotherapy, migration, invasion and dissemination in vivo. Our present study provides an understanding of how enhanced expression of miR-181a can confer malignant and invasive traits through the modulation of a canonical signaling pathway and a consequent maintenance of a mesenchymal state. Furthermore, inhibition of miR-181a led to a reversion of EMT and subsequent events through decreased TGF-β signaling. Our data confirmed Smad7 as a functional target through which TGF-β-mediated EMT occurs; re-expression of Smad7 lacking its 3'UTR was able to rescue miR-181a-mediated phenotypes, deeming Smad7 as a critical mediator of miR-181a-induced EMT. Other recent studies support the crucial role(s) that miRNAs play in mediating EMT and consequent aggressive disease traits. For example, the miR-106b-25 cluster has also been shown to target Smad7 and mediate TGF-β-induced EMT downstream to Six1 in breast cancer34. miR-9 directly targets E-cadherin and inhibition of miR-9 had led to an inhibition of metastasis35. Conversely, the miR-200 and -205 family was shown to target transcriptional repressors of E-cadherin, ZEB1 and SIP1, and re-expression of these miRNAs led to a mesenchymal-to-epithelial transition and prevented TGF-β -induced EMT36.

2013-12-01 | GSE52077 | GEO

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