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Comprehensive analysis of pathological changes in tumor of B16 with CCND1 overexpression

ABSTRACT: Comprehensive analysis of pathological changes in tumor of B16 with CCND1 overexpression

PROVIDER: PRJNA747836 | ENA |

REPOSITORIES: ENA

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Comprehensive analysis of pathological changes in tumor of B16 with CCND1 overexpression

Project description:Aims: CCND1 amplification was an unfavorable prognostic factor for patients with melanoma. This study aimed to investigate the molecular changes in tumor of B16 with CCND1 overexpression. Methods: High-throughput sequencing was used to identify genes that were differentially expressed in tumor between B16 controls and B16 with CCND1 overexpression. Tumors of B16 Ctrl (n=3) and B16 with CCND1 overexpression (n=3) were enrolled in this study. Results: mRNA expression of genes associated with immunity, such as CD8, Gzm, B2m, and Tap1 were decreased in tumors with CCND1 overexpression. Conclusion: CCND1 overexpression is associated with an immunosuppressive microenvironment.

2022-07-20 | GSE180327 | GEO

RNA sequencing analysis of B16-F1, B16-F1R2 and B16-F1R2L

Project description:We wanted to correlate the protein cargo of secreted exosomes with gene expression pattern in B16-F1 and B16-F1R2. For that purpose, we performed RNA sequencing analysis of B16-F1, B16-F1R2 and B16-F1R2L (Fig.1E). We identified >3000 genes significantly up-regulated and >1000 significantly down-regulated in B16-F1R2 model compared to B16-F1, using a false discovery rate (FDR) of 0.05.

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RNA sequencing analysis of B16-F1, B16-F1R2 and B16-F1R2L

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Profiling of differential RNAs in LY500307-treated B16 cells and control-treated B16 cells

Project description:In this study, we examined the differential RNA profile of LY500307-treated B16 cells compared with control-treated B16 cells

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proteomic analysis of B16-MDSCs

Project description:In order to analyse the B16-MDSCs proteome in a large-scale format, we used a multi-dimensional fractionation approach which combines peptide chromatographic fractionation strategies coupled to mass spectrometry.

2016-07-07 | PXD001103 | Pride

miroRNA sequencing of B16 cells and exosomes derived from B16 and JB6 cells

Project description:The goal of this study is to compare the miRNA profiles of melanoma cells B16-derived exosomes with B16 cells and normal cells JB6-derived exosomes.

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B16-F10 RNA-Seq

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Melan-a melanocytes and B16 melanoma cells

Project description:This SuperSeries is composed of the following subset Series: GSE11580: Time course RA-treatment of B16 mouse melanoma cells GSE11584: Melan-a mouse melanocytes vs. B16 mouse melanoma cells Keywords: SuperSeries Refer to individual Series

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Novel RNA-binding activity of MYF5 enhances Ccnd1/Cyclin D1 mRNA translation during myogenesis

Project description:Skeletal muscle contains long multinucleated and contractile structures known as muscle fibers, which arise from the fusion of myoblasts into nucleated myotubes during myogenesis. The myogenic regulatory factor (MRF) MYF5 is the earliest to be expressed during myogenesis and functions as a transcription factor in muscle progenitor cells (satellite cells) and myocytes. In mouse C2C12 myocytes, MYF5 is implicated in the initial steps of myoblast differentiation into myotubes. Ribonucleoprotein immunoprecipitation (RIP) analysis showed that MYF5 bound a subset of myoblast mRNAs; prominent among them was Ccnd1 mRNA, which encodes the key cell cycle regulator CCND1 (Cyclin D1). Biotin-RNA pulldown, UV-crosslinking, and gel shift experiments indicated that MYF5 was capable of binding the 3' untranslated region (UTR) and the coding region (CR) of Ccnd1 mRNA. MYF5 silencing in proliferating growing myoblasts revealed that and MYF5 promoted CCND1 translation, and it also modestly increased transcription of Ccnd1 mRNA. Importantly, silencing MYF5 reduced myoblast growth as well as differentiation of myoblasts into myotubes, while overexpressing MYF5 in C2C12 cells upregulated CCND1 expression. We propose that MYF5 enhances early myogenesis in part by coordinately elevating Ccnd1 transcription and Ccnd1 mRNA translation.

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