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Dropseq to study heterogeneity and tumorigenesis of Brca1-deficient mouse mammary tumors.

ABSTRACT: Dropseq to study heterogeneity and tumorigenesis of Brca1-deficient mouse mammary tumors.

PROVIDER: PRJNA625043 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11539705_1.fastq.gz	Fastqsanger.gz
	SRR11539705_2.fastq.gz	Fastqsanger.gz
	SRR11539706_1.fastq.gz	Fastqsanger.gz
	SRR11539706_2.fastq.gz	Fastqsanger.gz
	SRR11539707_1.fastq.gz	Fastqsanger.gz

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Dropseq to study heterogeneity and tumorigenesis of Brca1-deficient mouse mammary tumors.

Project description:Brca1 mutation predisposes women to early onset of breast and ovarian cancers.Through its diverse functions in DNA damage repair, cell cycle control, transcription regulation, ubiquitination and so on, BRCA1 acts as a very significant tumor suppressor and genomic safeguard. Brca1 deficiency induces severe cellular stress, when occurring in the mammary glands, it impairs the regular developmental process and eventually causes tumorigenesis due to accumulation of genome instability and other mechanisms. The Brca1-defiencient mouse mammary tumor were characterized with great tumoral heterogeneity, which is in line with the human breast cancers carrying BRCA1 mutations. Here we studied the molecular complexicity of Brca1-deficient mouse mammary tumors vie Dropseq.

2021-11-17 | GSE148566 | GEO

Single cell RNA-seq to study heterogeneity and tumorigenesis of Brca1-deficient mouse mammary tumors.

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Single cell RNA-seq to study heterogeneity and tumorigenesis of Brca1-deficient mouse mammary tumors.

Project description:Single cell RNA-seq to study heterogeneity and tumorigenesis of Brca1-deficient mouse mammary tumors.

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p16INK4a suppresses BRCA1-deficient mammary tumorigenesis.

Project description:Senescence prevents the proliferation of genomically damaged, but otherwise replication competent cells at risk of neoplastic transformation. p16INK4A (p16), an inhibitor of CDK4 and CDK6, plays a critical role in controlling cellular senescence in multiple organs. Functional inactivation of p16 by gene mutation and promoter methylation is frequently detected in human breast cancers. However, deleting p16 in mice or targeting DNA methylation within the murine p16 promoter does not result in mammary tumorigenesis. How loss of p16 contributes to mammary tumorigenesis in vivo is not fully understood.In this article, we reported that disruption of Brca1 in the mammary epithelium resulted in premature senescence that was rescued by p16 loss. We found that p16 loss transformed Brca1-deficient mammary epithelial cells and induced mammary tumors, though p16 loss alone was not sufficient to induce mammary tumorigenesis. We demonstrated that loss of both p16 and Brca1 led to metastatic, basal-like, mammary tumors with the induction of EMT and an enrichment of tumor initiating cells. We discovered that promoter methylation silenced p16 expression in most of the tumors developed in mice heterozygous for p16 and lacking Brca1. These data not only identified the function of p16 in suppressing BRCA1-deficient mammary tumorigenesis, but also revealed a collaborative effect of genetic mutation of p16 and epigenetic silencing of its transcription in promoting tumorigenesis. To the best of our knowledge, this is the first genetic evidence directly showing that p16 which is frequently deleted and inactivated in human breast cancers, collaborates with Brca1 controlling mammary tumorigenesis.

| S-EPMC5356676 | biostudies-literature

Attenuation of RNA polymerase II pausing mitigates BRCA1-associated R-loop accumulation and tumorigenesis.

Project description:Most BRCA1-associated breast tumors are basal-like yet originate from luminal progenitor cells. BRCA1 is best known for its functions in DNA repair and resolution of DNA replication stress. However, it is unclear whether loss of these ubiquitously important functions of BRCA1 fully explains the cell lineage-specific increase in breast tumor development. Cell culture-based studies implicate BRCA1 in elimination of R-loops, DNA-RNA hybrid structures involved in transcriptional regulation and genetic instability. We found that BRCA1 mutation-associated R-loop accumulates preferentially in luminal epithelial cells of cancer-free human breast tissue, and at the 5' end of those genes that experience promoter-proximal RNA polymerase II (Pol II) pausing. Genetic ablation of mouse NELF-B/COBRA1, a Pol II-pausing factor and BRCA1-binding protein, in Brca1 knockout mouse mammary epithelium ameliorates R-loop accumulation and reduces mammary tumorigenesis. Our studies show that Pol II pausing is a previously unappreciated contributor to BRCA1-associated R-loop accumulation and breast cancer development.

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Dissecting the heterogeneity and tumorigenesis of BRCA1 deficient mammary tumors via single cell RNA sequencing.

Project description:Background: BRCA1 plays critical roles in mammary gland development and mammary tumorigenesis. And loss of BRCA1 induces mammary tumors in a stochastic manner. These tumors present great heterogeneity at both intertumor and intratumor levels. Methods: To comprehensively elucidate the heterogeneity of BRCA1 deficient mammary tumors and the underlying mechanisms for tumor initiation and progression, we conducted bulk and single cell RNA sequencing (scRNA-seq) on both mammary gland cells and mammary tumor cells isolated from Brca1 knockout mice. Results: We found the BRCA1 deficient tumors could be classified into four subtypes with distinct molecular features and different sensitivities to anti-cancer drugs at the intertumor level. Whereas within the tumors, heterogeneous subgroups were classified mainly due to the different activities of cell proliferation, DNA damage response/repair and epithelial-to-mesenchymal transition (EMT). Besides, we reconstructed the BRCA1 related mammary tumorigenesis to uncover the transcriptomes alterations during this process via pseudo-temporal analysis of the scRNA-seq data. Furthermore, from candidate markers for BRCA1 mutant tumors, we discovered and validated one oncogene Mrc2, whose loss could reduce mammary tumor growth in vitro and in vivo. Conclusion: Our study provides a useful resource for better understanding of mammary tumorigenesis induced by BRCA1 deficiency.

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Project description:The transcriptional profile of WapCre;Rank;Brca1;p53 and WapCre;Brca1;p53 mouse primary mammary tumor cells was determined by mRNA sequencing and uncovered differences in their molecular signatures including genes involved in oncogenesis, basic metabolism, RNA metabolism, or the regulation of mammary stem cells.

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Transcription profiling of spontaneous and transplanted topotecan-resistant BRCA1;P53-deficient mouse mammary tumors

Project description:Gene expression profiles of "spontaneous" and transplanted topotecan-resistant BRCA1;P53-deficient mammary tumors and their matched untreated controls

2010-01-05 | E-NCMF-28 | biostudies-arrayexpress

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