Gene expression analysis of EuMyc lymphoma cells after MYC inactivation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA541945 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9030180_1.fastq.gz | Fastqsanger.gz | |||
| SRR9030180_2.fastq.gz | Fastqsanger.gz | |||
| SRR9030181_1.fastq.gz | Fastqsanger.gz | |||
| SRR9030181_2.fastq.gz | Fastqsanger.gz | |||
| SRR9030182_1.fastq.gz | Fastqsanger.gz |
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Project description:The oncogenic transcription factor (c-)Myc is overexpressed in a variety of cancers including subtypes of B cell lymphoma. Here we study long noncoding (lnc)RNAs regulated by Myc, arguing that these lncRNAs may be involved in the very strong effect of Myc on cell proliferation. Using multiple in vitro models and taking into account the kinetics of the response to Myc as well as Myc binding sites we defined two Myc-induced and four Myc-repressed lncRNA candidates. Expression levels of the top Myc-induced lncRNA KTN1-AS1 are low in normal B cell subsets and strongly increased in multiple Myc-positive lymphoma cell lines. In addition, primary lymphoma cases stratified by high or low Myc expression show the expected KTN1-AS1 expression differences. Knockdown of KTN1-AS1 severely impaired the cell growth of multiple Burkitt lymphoma cell lines. Gene expression analysis showed that KTN1-AS1 knockdown affects >300 genes genome wide with a strong enrichment of Myc-target genes involved in metabolism and biosynthesis. In line with this finding, KTN1-AS1 depletion in B cell lymphoma cells caused a substantial decrease of Myc transcript and protein. Thus, our data indicates that KTN1-AS1 overexpression in lymphoma may reinforce high Myc expression at the transcriptional level to activate gene expression programs supporting the high metabolic rate present in lymphoma cells. In conclusion, we identified a novel positive feedback loop between c-Myc and KTN1-AS1 in B cell lymphoma cells. LncRNAs such as KTN1-AS1, that regulate important oncogenic factors in specific cell types, may open new ways to cancer therapy.
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Project description:Myc is a well known transcription factor with important roles in cell cycle, apoptosis and cellular transformation. Long non-coding (lnc)RNAs have recently emerged as a important class of regulatory RNAs. Here, we show that lncRNAs are an extensive component of the Myc-regulated transcriptional program. Using the P493-6 inducible Myc model we demonstrate that both Myc-induced mRNAs and lncRNAs were significant enriched for Myc binding sites. In contrast to Myc-repressed mRNAs, Myc-repressed lncRNAs were significantly enriched for Myc binding sites. Subcellular localization analysis revealed that Myc-repressed lncRNAs and mRNAs are enriched in the nucleus while Myc-induced lncRNAs and mRNAs are enriched both in the cytoplasm and nucleus. Parallel analysis of differentially expressed lncRNAs and mRNAs identified 105 lncRNA-mRNA pairs that were in close vicinity, indicative for regulation in cis. To support the potential relevance of the Myc-regulated lncRNAs in cellular transformation, we analyzed their expression in primary Myc-high and Myc-low B-cell lymphomas. In total, 54% of the lncRNAs differentially expressed between the lymphoma subsets were identified as Myc-regulated in P493-6 cells. This study is the first to show that lncRNAs are an important factor within the Myc-regulated transcriptional program and indicates a marked difference between Myc-repressed lncRNAs and mRNAs. Expression of all known mRNAs and >10 000 lncRNAs was assessed in primary lymphoma tissue with high c-myc levels (Burkitt lymphoma; BL) and low c-myc levels (chronic lymphocytic leukemia; CLL)
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