RNA-seq profiling of C/EBPβ-overexpressing myoblasts
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA638154 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11955406.fastq.gz | Fastqsanger.gz | |||
| SRR11955407.fastq.gz | Fastqsanger.gz | |||
| SRR11955408.fastq.gz | Fastqsanger.gz | |||
| SRR11955409.fastq.gz | Fastqsanger.gz |
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Project description:We previously identified C/EBPβ as an inhibitor of myogenic differentiation and a regulator of muscle satellite cell self-renewal. We found that C/EBPβ is regulated during the transition from proliferation to growth arrest in myoblasts and overexpression of C/EBPβ in myoblasts promotes cell growth arrest in vitro and improves engraftment of satellite cells into the stem cell niche in vivo. To identify the molecular mechanism by which C/EBPβ regulates myoblast proliferation and growth arrest, we performed RNA-seq on C/EBPβ-overexpressing myoblasts.
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Project description:RNA-seq profiling of C/EBPβ-overexpressing myoblasts [proliferating myoblasts]
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Project description:C/EBPβ (CCAAT enhancer binding protein) is a transcription factor that plays a crucial role in survival and transformation of ALK+ anaplastic large cell lymphoma (ALCL). The aim of this study was to identify the downstream targets of C/EBPβ responsible for ALK-mediated oncogenesis. C/EBPβ was knocked down in ALK+ ALCL cell lines with a C/EBPβ-shRNA, followed by gene expression profiling (GEP). GEP analysis revealed a reproducible signature of genes that were significantly regulated by C/EBPβ. Classification into biological categories revealed overrepresentation of genes involved in the immune response, apoptosis and cell proliferation. Transcriptional regulation by C/EBPβ was found in 6 of 11 (BCL2A1, G0S2, TRIB1, S100A9, DDX21 and DDIT4) genes investigated by chromatin immunoprecipitation. We demonstrated that BCL2A1, G0S2 and DDX21 play a crucial role in survival and proliferation of ALK+ ALCL cells. DDX21, a gene involved in rRNA biogenesis, was found differentially overexpressed in primary ALK+ ALCL cases. All three candidate genes were validated in primary ALCL cases by either immunohistochemistry or RT-qPCR. In conclusion, we identified and validated several key C/EBPβ-regulated genes with major impact on survival and cell growth in ALK+ ALCL, supporting the central role of C/EBPβ in ALK-mediated oncogenesis. Kijk and SUDHL1 cell lines transfected with shRNA for C/EBPbeta were compared to control cells (3 biological replicates per group) and untreated cells (1 biological replicate)
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