Cuttag sequencing revealed the regulatory targets of transcription factor c-MYC in human chondrocytes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1127618 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29528678_1.fastq.gz | Fastqsanger.gz | |||
| SRR29528678_2.fastq.gz | Fastqsanger.gz | |||
| SRR29528679_1.fastq.gz | Fastqsanger.gz | |||
| SRR29528679_2.fastq.gz | Fastqsanger.gz |
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Project description:The transcription factor MYC can promote chondrocyte differentiation in previous studies, but its target remains unclear. We used cutt sequencing to explore its regulatory targets.
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Project description:b'MYC is an oncoprotein transcription factor that is overexpressed in the majority cancers. Although MYC itself is considered undruggable, it may be possible to inhibit MYC by targeting the co-factors it uses to drive oncogenic gene expression patterns. Here, we use loss- and gain- of function approaches to interrogate how one MYC co-factorHost Cell Factor (HCF)-1contributes to MYC activity in a Burkitt lymphoma setting. We identify high-confidence direct targets of the MYCHCF-1 interaction that are regulated through a recruitment-independent mechanism, including genes that control mitochondrial function and rate-limiting steps for ribosome biogenesis and translation. We describe how these gene expression events impact cell growth and metabolism, and demonstrate that the MYCHCF-1 interaction is essential for tumor maintenance in vivo. This work highlights the MYCHCF-1 interaction as a focal point for development of novel anti-cancer therapies.'
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