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:Tumors that overexpress the MYC oncogene frequently demonstrate aneuploidy, numerical chromosome alterations associated with highly aggressive cancers, rapid tumor evolution, and poor patient outcome. Here, we identify that MYC overexpression induces defects in microtubule nucleation and mitotic spindle assembly, promoting chromosome segregation defects, micronuclei and chromosomal instability (CIN). High TPX2 expression is permissive for mitotic spindle assembly and chromosome segregation in cells with MYC overexpression; whereas TPX2 depletion blocks mitotic progression, induces cell death and prevents tumor growth. Attenuating MYC expression reverses mitotic defects, even in established tumor cell lines, implicating an ongoing role for high MYC in the persistence of CIN in tumors. Our studies implicate the MYC oncogene as a regulator of spindle assembly and identify a new MYC-TPX2 synthetic-lethal interaction that could represent a future therapeutic strategy in MYC-overexpressing cancers. Moreover, our studies suggest that blocking MYC activity can attenuate the emergence of CIN and tumor evolution.
2020-03-30 | GSE130920 | GEO
Project description:Gene expression in murine T-ALL following MYC inactivation
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Project description:To understand changes to gene expression in murine T-ALL following MYC inactivation, T-ALL cells were isolated from EμSRα-tTA/tet-O-MYC/FVB/N mice and treated with varying concentrations of doxycyline for 48 hours to place cells in the MYC on, MYC intermediate, or MYC off state.
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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.
2020-04-03 | GSE119924 | GEO
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)
2015-02-01 | E-GEOD-59479 | biostudies-arrayexpress
Project description:Gene expression in murine T-ALL following titrated MYC inactivation
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Project description: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-factor—Host Cell Factor (HCF)-1—contributes to MYC activity in a Burkitt lymphoma setting. We identify high-confidence direct targets of the MYC–HCF-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 MYC–HCF-1 interaction is essential for tumor maintenance in vivo. This work highlights the MYC–HCF-1 interaction as a focal point for development of novel anti-cancer therapies.
2020-07-15 | ST001429 | MetabolomicsWorkbench
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:To understand changes to gene expression over time in murine T-ALL following MYC inactivation, T-ALL cells were isolated from EμSRα-tTA/tet-O-MYC/FVB/N mice and treated with doxycyline to turn MYC off for varying amounts of time before assessing gene expression.
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Project description:This SuperSeries is composed of the following subset Series: GSE12278: MYC stimulates EZH2 expression by repression of its negative regulator miR-26a GSE12394: murine MYC-dependent lymphoma cells: Dox vs. NoDox treatment Refer to individual Series
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