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The effect of c-Myc over-expression on the sensitivity to Tipifarnib treatment in three cancer cell lines

ABSTRACT: The effect of c-Myc over-expression on the sensitivity to Tipifarnib treatment in three cancer cell lines

PROVIDER: PRJNA863472 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20706872_1.fastq.gz	Fastqsanger.gz
	SRR20706872_2.fastq.gz	Fastqsanger.gz
	SRR20706873_1.fastq.gz	Fastqsanger.gz
	SRR20706873_2.fastq.gz	Fastqsanger.gz
	SRR20706874_1.fastq.gz	Fastqsanger.gz

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The effect of c-Myc over-expression on the sensitivity to Tipifarnib treatment in three cancer cell lines

Project description:To investigate whether the over-expression of c-Myc gene can sensitize cancer cells of multiple tissue origins to Tipifarnib. We performed differential gene expression analysis using RNA-seq profile of three c-Myc over-expressed and control cell lines with/without Tipifarnib treatment.

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MYC, together with Cohesin and Mediator complexes, predetermines the sensitivity of gastrointestinal cancer to antifolate drugs

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MYC family amplification dictates sensitivity to BET bromodomain protein inhibitor Mivebresib (ABBV-075) in small cell lung cancer

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Long-range enhancer activity determines Myc sensitivity to Notch inhibitors in T cell leukemia

Project description:Notch is needed for T cell development and is a common oncogenic driver in T cell acute lymphoblastic leukemia. Myc is a critical target of Notch in normal and malignant pre-T cells, but how Notch regulates Myc is unknown. Here, we identify a distal enhancer located >1 Mb 3' of human and murine Myc that binds Notch transcription complexes and physically interacts with the Myc proximal promoter. The Notch1 binding element in this region activates reporter genes in a Notch-dependent, cell context-specific fashion that requires a conserved Notch complex binding site. Acute changes in Notch activation produce rapid changes in H3K27 acetylation across the entire enhancer (a region spanning >600 kb) that correlate with Myc expression. This broad Notch-influenced region is comprised of an enhancer region containing multiple domains, recognizable as discrete H3K27 acetylation peaks. Leukemia cells selected for resistance to Notch inhibitors express Myc despite epigenetic silencing of enhancer domains near the Notch transcription complex binding sites. Notch-independent expression of Myc in resistant cells is highly sensitive to inhibitors of Brd4, a change in drug sensitivity that is accompanied by preferential association of the Myc promoter with more 3’ enhancer domains that are strongly dependent on Brd4 for function. These findings indicate that altered long-range enhancer activity can mediate resistance to targeted therapies and provide a mechanistic rationale for combined targeting of Notch and Brd4 in leukemia.

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Project description:MYC and hypoxia gene clusters are the two most commonly recurring transcriptional programs in heterogenous tumors. Understanding the cellular fitness of MYC-driven cancer cells in normoxia and hypoxia may lead to identification of distinct cancer cell vulnerabilities. Using genome-wide CRISPR screenings of MYC-driven liver cancer cells cultured over 4 weeks in 21% and 1% oxygen in monolayer, and 21% oxygen in 3D spheroid, we not only identify over 600 essential genes under all three conditions but also context-specific fitness genes and pathways. Knockout of VHL-HIF1 pathway results in incompatible fitness defects under 21% oxygen versus 1% oxygen or 3D. Genetic deletion of each of the mitochondrial respiratory complex I-V has distinct cellular fitness outcomes. Notably, the organogenesis signaling pathways such as TGF-SMAD specifically limits the uncontrolled cell proliferation of 3D spheroids while inactivation of epigenetic modifiers (Bcor, Kmt2d, Mettl3 and Mettl14) has opposite outcomes in monolayer versus 3D. We also discover distinct metabolic requirement for fatty acid and cholesterol synthesis in three conditions. Chemical perturbations using 125 FDA approved oncology drugs reveal that MYC-driven liver cancer cells have different sensitivity to inhibition of tyrosine kinase receptors under hypoxia and 3D. Our resource study highlights unique epigenetic and metabolic dependency of MYC-driven cancer cells in different tumor environmental settings.

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Ectopic Myc expression

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Comparing mRNA expression between carrier treated and sorafenib treated Myc/NrasG12V liver tumors

Project description:To profile determinants of sensitivity and resistance towards the multikinase inhibitor sorafenib in liver cancer (HCC), we generated HCCs with elevated MYC expression and activated Raf-MEK-ERK signaling. To trigger tumor development, we co-delivered transposable elements encoding for Myc and oncogenic NrasG12V via hydrodynamic injection into the hepatocytes of C57BL/6 wildtype mice. To characterize the response of Myc/NrasG12V HCCs towards sorafenib, we analyzed their transcriptomes after three weeks of sorafenib or carrier treatment.

2020-12-01 | GSE162322 | GEO

Transcription profiling of mouse colon carcinomas over-expressing c-Myc

Project description:MycRas vs Ras colon carcinoma. Human adenocarcinomas commonly harbor mutations in the Ki-Ras and c-Myc proto-oncogenes and the trp53 tumor suppressor gene. All three genetic lesions are potentially pro-angiogenic, since they sustain production of the vascular endothelial growth factor (VEGF). Yet murine Ki-Ras/p53-null colonocytes formed indolent, poorly vascularized tumors, whereas additional transduction with a Myc-encoding retrovirus promoted vigorous vascularization and growth. While VEGF levels were unaffected by Myc, enhanced neovascularization correlated with down-regulation of anti-angiogenic thrombospondin-1 (Tsp1) and related proteins, such as connective tissue growth factor (CTGF). Both Tsp1 and CTGF are predicted targets for repression by the miR-17-92 microRNA cluster, which was upregulated in RasMyc colonocytes. Indeed, miR-17-92 knock-down with antisense 2’-O-methyl oligoribonucleotides partly restored Tsp1 and CTGF expression, and conversely, transduction of Ras-only cells with a miR-17-92-encoding retrovirus reduced Tsp1 and CTGF levels. Importantly, miR-17-92-transduced cells formed larger, better perfused tumors. These findings establish a role for microRNAs in non-cell-autonomous Myc-induced tumor phenotypes.

2006-09-08 | E-MEXP-757 | biostudies-arrayexpress

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