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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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			Action	DRS
	SRR15184008_1.fastq.gz	Fastqsanger.gz
	SRR15184008_2.fastq.gz	Fastqsanger.gz
	SRR15184009_1.fastq.gz	Fastqsanger.gz
	SRR15184009_2.fastq.gz	Fastqsanger.gz
	SRR15184010_1.fastq.gz	Fastqsanger.gz

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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

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

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B16 versus B16B1

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proteomic analysis of B16-MDSCs

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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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B16-F10 RNA-Seq

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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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