Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA369806 | ENA |
REPOSITORIES: ENA
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Project description:Context-dependent miR-204 and miR-211 affect the biological properties of amelanotic and melanotic melanoma cells
| PRJNA369800 | ENA
Project description:Context-dependent miR-204 and miR-211 affect the biological properties of amelanotic and melanotic melanoma cells [miRNA-Seq]
| PRJNA369664 | ENA
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: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:MicroRNAs (miRNAs) influence cancer development through post-transcriptional negative regulation of both tumor suppressors and oncogenes. We subjected melanoma cell lines, normal melanocytes, and keratinocytes to array based miRNA profiling, and identified several distinct miRNAs with differential expression. Specifically, miR-211 levels were depleted in all eight melanoma cell lines examined, and also in 23 of 30 distinct patient melanoma samples (graded as primary in situ, regional metastatic, distant metastatic and nodal metastatic). Putative target genes of miR-211 were identified, and their anticipated increased expression levels were confirmed in melanoma cell lines, which were reduced in two melanoma cell lines that artificially over-expressed miR-211. Four such target genes (TCF12, RAB22A, KCNMA1 and SLC37A3) were confirmed by a target cleavage assay. Stable over-expression of miR-211 in two melanoma cell lines caused significant growth inhibition and reduced invasiveness. The differential expression of miR-211 in a variety of melanoma cell lines and clinical samples, consistent inverse correlation between miR-211 and its target mRNA levels, and growth retardation and reduced invasiveness of melanoma cell lines by miR-211 are all consistent with the idea that the depletion of miR-211 is a key step in melanoma development and/or progression
2009-12-31 | GSE15281 | 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
Project description:Using the highly sensitive miRNA array, we screened 220 microRNAs abundant in physiological left ventricular hypertrophy (LVH) and we explored the functions of these miRNAs in the cardiac tissue by Gene Ontology and Kyoto Encyclopedia of Genes annotation. miRNAs showed a high score in the pathway enriched in autophagy. Moreover, the expression levels of miR-26b-5p, miR-204-5p, and miR-497-3p showed an obvious increase in rat hearts. Adenovirus-mediated overexpression of miR-26b-5p, miR-204-5p, and miR-497-3p markedly attenuated IGF-1-induced hypertrophy in H9C2 cells by suppressing autophagy. Furthermore, miR-26b-5p, miR-204-5p, and miR-497-3p attenuated autophagy in H9C2 cells through targeting ULK1, LC3B and Beclin 1, respectively. Taken together, our results demonstrate that swimming exercise induced physiological LVH, at least in part, by modulating the microRNA–autophagy axis, and that miR-26b-5p, miR-204-5p, and miR-497-3p may help distinguish physiological and pathological LVH.
2020-01-21 | GSE143935 | GEO