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RNA sequencing (RNA-SEQ) of HMGA1 knockdown by shRNA in cholangiocarcinoma cells

ABSTRACT: RNA sequencing (RNA-SEQ) of HMGA1 knockdown by shRNA in cholangiocarcinoma cells

PROVIDER: PRJNA687481 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13293004_1.fastq.gz	Fastqsanger.gz
	SRR13293004_2.fastq.gz	Fastqsanger.gz
	SRR13293005_1.fastq.gz	Fastqsanger.gz
	SRR13293005_2.fastq.gz	Fastqsanger.gz
	SRR13293006_1.fastq.gz	Fastqsanger.gz

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RNA sequencing (RNA-SEQ) of HMGA1 knockdown by shRNA in cholangiocarcinoma cells

Project description:Cholangiocarcinoma (CHOL) is a malignancy arising from either the intrahepatic or the extrahepatic bile ducts which carries a severe prognosis. HMGA1 is a transcription factor which has a high expression level in many types of cancer. In this study, we find HMGA1 overexpression in CHOL. In order to investigate the regulatory mechanism of HMGA1 in CHOL, we performed RNA-seq in HUCCT1 cells with HMGA1 knock down compared with control in three repeat.

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Project description:Emerging evidence suggests that tumor cells metastasize by co-opting stem cell transcriptional networks, although the molecular underpinnings of this process are poorly understood. Here, we show for the first time that the high mobility group A1 (HMGA1) gene drives metastatic progression in triple negative breast cancer cells (MDA-MB-231) by reprogramming cancer cells to a stem-like state. We discovered an HMGA1 signature in triple negative breast cancer cells that is highly enriched in embryonic stem cells. Together, these findings indicate that HMGA1 is a master regulator of tumor progression in breast cancer by reprogramming cancer cells through stem cell transcriptional networks. Future studies are needed to determine how to target HMGA1 in therapy. HMGA1 was knocked-down in MDA-MB-231 cells using siRNA as we previously described (Tesfaye A 2007). RNA from three independent knockdown experiements along with 3 control populations were collected by Rneasy miniprep (Qiagen) and analyzed by Affymetrix Human Exon 1.0 ST platform.

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