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Elucidating and Pharmacologically Targeting Master Regulators of Stem-like Breast Cancer Cell State (CROP-Seq)

ABSTRACT: Elucidating and Pharmacologically Targeting Master Regulators of Stem-like Breast Cancer Cell State (CROP-Seq)

PROVIDER: PRJNA1006414 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25678743_1.fastq.gz	Fastqsanger.gz
	SRR25678743_2.fastq.gz	Fastqsanger.gz
	SRR25678744_1.fastq.gz	Fastqsanger.gz
	SRR25678744_2.fastq.gz	Fastqsanger.gz
	SRR25678745_1.fastq.gz	Fastqsanger.gz

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Elucidating and Pharmacologically Targeting Master Regulators of Stem-like Breast Cancer Cell State

Project description:Elucidating and Pharmacologically Targeting Master Regulators of Stem-like Breast Cancer Cell State

| PRJNA939709 | ENA

Elucidating and Pharmacologically Targeting Master Regulators of Stem-like Breast Cancer Cell State (CROP-Seq)

Project description:In many tumors, small subpopulations of stem-like cells can exist in drug-resistant states that are transient and epigenetically governed. Single-cell RNA sequencing (scRNA-seq) provides transcriptional profiles for individual cells which, although sparse and noisy, may provide insight into how they are regulated and how they may be targeted. We took a systems-biology approach to analyzing cancer stem-like cells (CSLCs) in breast tumors and predicting Master Regulator (MR) proteins responsible for governing the transcriptional state of these cells, thus revealing drug sensitivities that may be leveraged via combination therapy. The MRs were validated by pooled, CRISPR-KO mediated CROP-seq profiling of single cells representing either the CLSC or the differentiated breast cancer (BRCA) cells.

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Elucidating and Pharmacologically Targeting Master Regulators of Stem-like Breast Cancer Cell State

Project description:In many tumors, small subpopulations of stem-like cells can exist in drug-resistant states that are transient and epigenetically governed. Single-cell RNA sequencing provides transcriptional profiles for individual cells which, although sparse and noisy, may provide insight into how they are regulated and how they may be targeted. We took a systems-biology approach to analyzing stem-like cells in breast tumors and predicting how this drug-resistant subpopulation might be sensitized to treatment. Our analysis predicted that the anthelmintic albendazole would reprogram the stem-like population, and a subsequent sensitizing-then-kill experiment in triple negative breast cancer PDX mice revealed a synergistic relationship between albendazole and the first-line treatment, paclitaxel. These results are a proof of concept that it is possible to use, a systems biology approach to identify drugs that can reprogram cell-state, and that tumor subpopulations which have long been considered intractable may be forced into a sensitive state.

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P-stalk ribosomes act as master regulators of cytokine-mediated processes

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Cistrome-partitioning reveals convergence of somatic mutations and risk-variants on master transcription regulators in primary prostate tumors

Project description:Thousands of noncoding somatic Single Nucleotide Variants (SNVs) of unknown function are reported in tumors. Partitioning the genome according to cistromes, reveals the enrichment of somatic SNVs in prostate tumors as opposed to adjacent normal tissue cistromes of master transcription regulators, including AR, FOXA1 and HOXB13. This parallels enrichment of prostate cancer genetic predispositions over these transcription regulators’ tumor cistromes, exemplified at the 8q24 locus harboring both risk-variants and somatic SNVs in cis-regulatory elements, upregulating MYC expression and altering the binding of transcription regulators to DNA. However, Massively-Parallel Reporter Assays reveal that few SNVs can alter the transactivation potential of individual CREs. Instead, SNVs accumulate, similarly to inherited riskvariants, in cistromes of master transcription regulators required for prostate cancer development. Difficulties in inferring the biological significance of noncoding mutations have limited their inclusion in precision genomics medicine pipelines. Most attempts to delineate a role for noncoding mutations relied on detecting evidence for positive selection within individual CREs, such as reported for the TERT gene promoter. By considering the enrichment of noncoding mutations in cistromes as opposed to individual CREs, we reveal their specificity towards master transcription regulators that promote prostate cancer development, a feature shared with inherited risk-variants. Overall, our work provides a blueprint for the functional interpretation of noncoding mutations in genomic tests relying on defining cis-regulatory units according to cistrome-partitioning to identify cancer driver transcription regulators.

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