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Global transcriptional responses to KI-MS2-008 treatment and Myc inactivation via doxycycline addition

ABSTRACT: Global transcriptional responses to KI-MS2-008 treatment and Myc inactivation via doxycycline addition

PROVIDER: PRJNA419363 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6313430.fastq.gz	Fastqsanger.gz
	SRR6313440.fastq.gz	Fastqsanger.gz
	SRR6313450.fastq.gz	Fastqsanger.gz
	SRR6313460.fastq.gz	Fastqsanger.gz
	SRR6313470.fastq.gz	Fastqsanger.gz

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Global transcriptional responses to KI-MS2-008 treatment and Myc inactivation via doxycycline addition

Project description:The Myc/Max heterodimer has crucial roles in normal cellular processes such as cell proliferation, metabolism, apoptosis, and differentiation, but its activity is often deregulated in a majority of human cancers. In an effort to explore alternative modes of Myc perturbation, we identified KI-MS2-008 as a small molecule that binds Max and modulates Myc-driven transcription, and in some cellular contexts, KI-MS2-008 treatment leads to a decrease in c-Myc protein levels. As the Myc/Max heterodimer controls many cellular processes, we expected that treatment with this small molecule would cause changes in the transcriptome. We found that treatment with 10 µM KI-MS2-008 resulted in global alterations in the transcriptome, mimicking direct Myc inactivation with doxycycline in P493-6, a B cell line with a Tet-Off system for c-Myc expression. We also discovered enrichment of various Myc target gene sets in the genes downregulated in response to KI-MS2-008 treatment in P493-6 cells. This trend was also observed in ST486 cells, but not in P3HR1 cells, which were chosen as non-engineered B cell lines that were sensitive and insensitive, respectively, toward KI-MS2-008 in cell viability assays.

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