Deletion of miR-204 and miR-211 in murine retinal pigment epithelium results in slow retinal degeneration
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PROVIDER: PRJNA1076855 | ENA |
REPOSITORIES: ENA
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Project description:To determine the gene expression changes in the retina of miR-204/miR-211 RPE conditional knockout (dKO) mice, we collected retina samples from dKO and controls animals at 6 months of degeneration, generated single-cell suspensions, and created scRNA-seq libraries (Parse Biosciences), and sequened the libraries.
2024-06-05 | GSE255851 | GEO
Project description:Purpose: Identification of miRNAs that enable resistance to BRAF inhibitors in melanoma suggests a mechanism-based strategy to limit resistance and improve clinical outcomes. Methods: We generated A375 melanoma cells resistant to Vemurafenib (VMF) with the goal of investigating changes in miRNA expression patterns that might contribute to resistance. Results: Increased expression of miR-204-5p and miR-211-5p occurring in VMF-resistant cells was determined to impact VMF response.
2018-01-18 | GSE107576 | GEO
Project description:Despite increasing amounts of experimental evidence depicting the involvement of non-coding RNAs in cancer, the study of BRAFV600E-regulated genes has thus far focused mainly on protein-coding ones. Here, we identify and study the microRNAs that BRAFV600E regulates through the ERK pathway. By performing small RNA sequencing on A375 melanoma cells and a vemurafenib- resistant clone that was taken as negative control, we discover miR-204 and miR-211 as the miRNAs most induced by vemurafenib. We also demonstrate that, although belonging to the same family, these two miRNAs have distinctive features. miR-204 is under the control of STAT3 and its expression is induced in amelanotic melanoma cells, where it acts as an effector of vemurafenib’s anti-motility activity by targeting AP1S2. Conversely, miR-211, a known transcriptional target of MITF, is induced in melanotic melanoma cells, where it targets EDEM1 and consequently impairs the degradation of TYROSINASE (TYR) through the ER-associated degradation (ERAD) pathway. In doing so, miR-211 serves as an effector of vemurafenib’s pro-pigmentation activity. We also show that such an increase in pigmentation in turn represents an adaptive response that needs to be overcome using appropriate inhibitors in order to increase the ef cacy of vemurafenib. In summary, we unveil the distinct and context-dependent activities exerted by miR-204 family members in melanoma cells. Our work challenges the widely accepted “same miRNA family = same function” rule and provides a rationale for a novel treatment strategy for melanotic melanomas that is based on the combination of ERK pathway inhibitors with pigmentation inhibitors.
2017-03-26 | GSE94476 | GEO
Project description:Despite increasing amounts of experimental evidence depicting the involvement of non-coding RNAs in cancer, the study of BRAFV600E-regulated genes has thus far focused mainly on protein-coding ones. Here, we identify and study the microRNAs that BRAFV600E regulates through the ERK pathway. By performing small RNA sequencing on A375 melanoma cells and a vemurafenib- resistant clone that was taken as negative control, we discover miR-204 and miR-211 as the miRNAs most induced by vemurafenib. We also demonstrate that, although belonging to the same family, these two miRNAs have distinctive features. miR-204 is under the control of STAT3 and its expression is induced in amelanotic melanoma cells, where it acts as an effector of vemurafenib’s anti-motility activity by targeting AP1S2. Conversely, miR-211, a known transcriptional target of MITF, is induced in melanotic melanoma cells, where it targets EDEM1 and consequently impairs the degradation of TYROSINASE (TYR) through the ER-associated degradation (ERAD) pathway. In doing so, miR-211 serves as an effector of vemurafenib’s pro-pigmentation activity. We also show that such an increase in pigmentation in turn represents an adaptive response that needs to be overcome using appropriate inhibitors in order to increase the ef cacy of vemurafenib. In summary, we unveil the distinct and context-dependent activities exerted by miR-204 family members in melanoma cells. Our work challenges the widely accepted “same miRNA family = same function” rule and provides a rationale for a novel treatment strategy for melanotic melanomas that is based on the combination of ERK pathway inhibitors with pigmentation inhibitors.
2017-03-26 | GSE94423 | GEO
Project description:Genome-wide expression analysis of MCF-10A and MCF-7 where miR-204 and miR-211 are overexpressed. The characteristics of differentially expressed genes in both cell lines derives the cells toward being oncogenic.
2016-05-23 | GSE75292 | GEO
Project description:Transcriptome profile of retinas from wild-type (c57BL/6) and RHO-P347S mice following AAV-mediated subretinal delivery of pre-miR-204 to study the molecular changes underlying the neuroprotective effect of miR-204 OE in mouse models of Inherited Retinal Disease (IRD) To determine the molecular changes associated with AAV-mediated delivery of miR-204 in the subretinal space of wild-type and IRD mouse models, we performed RNASeq analysis of retinas from c57BL/6 and RHO-P347S mice injected with the AAV2/8.CMV.miR204 and AAV2/8.CMV.miR204MUT vector in a paired manner.
2019-12-02 | GSE121785 | GEO
Project description:miR-204-5p and miR-211-5p contribute to BRAF inhibitor resistance in melanoma
| PRJNA420730 | ENA
Project description:The aim of this study is to discover genes regulated by miR-204. Differential gene expression in HEK-293 cells transfected with miR-204-mimic compared to HEK-293 cells transfected with control oligo (HEK-293 control) was analyzed using the Agilent Human Whole Genome 4x44K gene expression array (Agilent Technologies, Santa Clara, CA). HEK-293 cells were transfected with either miR-204 or a control, and gene expression was analyzed using the Agilent Human Whole Genome 4x44K array. A dye-swap was performed.
2012-03-30 | E-GEOD-28400 | biostudies-arrayexpress
Project description:Introduction: The mechanisms underlying myopia and myopia-related retinopathy remain not fully understood. We proposed to examine the function and underlying mechanisms of miR-204-5p in myopia development. Methods: The miR-204-5p expression level was assessed in the vitreous humor (VH) of a cohort consisting of 11 patients with high myopia (HM) and 16 control patients undergoing retinal surgery. The functional implications of miR-204-5p in ARPE-19 cells were assessed, encompassing cell aggressiveness. Thioredoxin-interacting protein (TXNIP) was found as a possible target of miR-204-5p through mRNA sequencing, and its interaction with miR-204-5p was confirmed employing luciferase assay and western blotting. Furthermore, the miR-204-5p function in regulating oxidative stress was examined by measuring reactive oxygen species (ROS) accumulation. Results: miR-204-5p was found to be significantly reduced in the VH of HM patients. Overexpression of miR-204-5p suppressed cell proliferation, migration, invasion, and apoptosis in ARPE-19 cells. The bioinformatics analysis demonstrated that miR-204-5p can modulate the genes associated with pathways relevant to myopia, including glycosaminoglycan (GAG) degradation, lysosome, and TGF−beta signaling pathway. The direct targeting of miR-204-5p on TXNIP has been confirmed through validation, and its downregulation mediated the miR-204-5p impacts on ARPE-19 cells. Moreover, miR-204-5p overexpression significantly reduced ROS accumulation by targeting TXNIP. Conclusion: Our findings revealed the possible contribution of the miR-204-5p/TXNIP axis in myopia development by regulating oxidative stress, which may provide new targets and novel therapeutic strategies to combat this prevalent and debilitating condition.
2024-01-26 | GSE253960 | GEO
Project description:The aim of this study is to discover genes regulated by miR-204. Differential gene expression in HEK-293 cells transfected with miR-204-mimic compared to HEK-293 cells transfected with control oligo (HEK-293 control) was analyzed using the Agilent Human Whole Genome 4x44K gene expression array (Agilent Technologies, Santa Clara, CA).
2012-03-31 | GSE28400 | GEO