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RNA-seq of nulliparus Robo1+/+ and Robo1-/- luminal progenitors

ABSTRACT: RNA-seq of nulliparus Robo1+/+ and Robo1-/- luminal progenitors

PROVIDER: PRJNA691604 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13422579_1.fastq.gz	Fastqsanger.gz
	SRR13422579_2.fastq.gz	Fastqsanger.gz
	SRR13422580_1.fastq.gz	Fastqsanger.gz
	SRR13422580_2.fastq.gz	Fastqsanger.gz
	SRR13422581_1.fastq.gz	Fastqsanger.gz

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RNA-seq of nulliparus Robo1+/+ and Robo1-/- luminal progenitors

Project description:The goal of the study was to compare gene expression of Robo1+/+ and Robo1-/- luminal progenitors. Total RNAs were then extracted from FACS purified luminal progenitor cells, harvested from Robo1+/+ or Robo1-/- mice (n=3 per genotype, two animals per n) using TRIreagent LS (Sigma, T3934). Poly(A)+ RNA sequencing libraries were made from each sample using the TruSeq RNA library preparation kit v.1 (Illumina). Illumina RNA PolyA library preparation guide. A total of 6 libraries were created by PCR amplification with Illumina barcoding primers using kit recommended conditions and quantified using a Bioanalyzer DNA 1000 kit (Agilent).

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Ductal keratin 15+ luminal progenitors in normal breast exhibit a basal-like breast cancer transcriptomic signature

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Transcriptomic profiling of 4T1 cells depleted for Id1/3 and Robo1

Project description:Id1 and its closely related family member Id3 are expressed by a diversity of stem and progenitor cells. We show that Id1/3 are required for the self-renewal and proliferation of triple negative breast cancer (TNBC) cells both in vitro and in vivo. Furthermore, we identified that Id1/3 negatively regulates the tumour suppressor gene Robo1. Depletion of Robo1 could rescue the proliferative defect induced by Id1/3 knockdown. To understand the mechanisms by which Robo1 rescues cell proliferation in Id1/3 depleted cells, we performed RNA-Sequencing on 4T1 cells with Dox-inducible Id1/3 KD and/or Robo1 depletion using siRNA. We conclude that following Id1/3 knockdown, Robo1 is induced and exerts anti-proliferative effects via suppression of a Myc transcriptional program.

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