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Homo sapiens

ABSTRACT: Effect of Hotair overexpression in human breast cancer cell lines

PROVIDER: PRJNA294267 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2218140_1.fastq.gz	Fastqsanger.gz
	SRR2218140_2.fastq.gz	Fastqsanger.gz
	SRR2218141_1.fastq.gz	Fastqsanger.gz
	SRR2218141_2.fastq.gz	Fastqsanger.gz
	SRR2218142_1.fastq.gz	Fastqsanger.gz

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Effect of Hotair overexpression in human breast cancer cell lines

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Transcriptome analysis of inducible HOTAIR overexpression mouse breast cancer cells

Project description:HOTAIR is a 2.2 kb long noncoding RNA (lncRNA) whose dysregulation has been linked to oncogenesis, defects in pattern formation during early development, and irregularities during the process of epithelial-to-mesenchymal transition (EMT). However, the oncogenic transformation determined by HOTAIR in vivo and its impact on chromatin dynamics are incompletely understood. Here we generate a transgenic mouse model with doxycycline-inducible expression of human HOTAIR in the context of the MMTV-PyMT breast cancer-prone background (iHOT-PyMT mice) to systematically interrogate the cellular mechanisms by which human HOTAIR lncRNA acts to promote breast cancer progression. We isolated breast cancer cells from the primary tumors of iHOT-PyMT mice (named iHOT+ cells) and performed RNA-seq and ATAC-seq of iHOT+ cells treated with 3 conditions: Dox+, Dox- and DoxWD. We showed that HOTAIR overexpression altered both the cellular transcriptome and chromatin accessibility landscape of multiple metastasis-associated genes and promoted epithelial to mesenchymal transition. These alterations are abrogated within several cell cycles after HOTAIR expression is reverted to basal levels, indicating an erasable lncRNA-associated epigenetic memory. These results suggest that a continual role for HOTAIR in programming a metastatic gene regulatory program.

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