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Tissue-specific transcription reprogramming promotes liver metastasis of colorectal cancer (ChIP-Seq)

ABSTRACT: Tissue-specific transcription reprogramming promotes liver metastasis of colorectal cancer (ChIP-Seq)

PROVIDER: PRJNA418457 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6293160.fastq.gz	Fastqsanger.gz
	SRR6293161.fastq.gz	Fastqsanger.gz
	SRR6293162.fastq.gz	Fastqsanger.gz
	SRR6293163.fastq.gz	Fastqsanger.gz
	SRR6293164.fastq.gz	Fastqsanger.gz

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Tissue-specific transcription reprogramming promotes liver metastasis of colorectal cancer

Project description:Tissue-specific transcription reprogramming promotes liver metastasis of colorectal cancer

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Tissue-specific transcription reprogramming promotes liver metastasis of colorectal cancer (ChIP-Seq)

Project description:Metastasis is the cause of death for 90% of cancer patients, but little is known about how cancer cells adapt to and colonize new tissue environments. Using clinical samples and primary/metastatic cell lines, we found metastatic colorectal cancer (CRC) cells lose their colon-specific gene transcription program and gain a liver-specific gene transcription program as they metastasize in the liver. We revealed this transcription reprogramming is driven by a reshaped epigenetic landscape of both typical and super-enhancers. Further, we identified FOXA2, a liver-specific transcription factor, plays a key role in this transcription reprogramming and the colonization of metastatic CRC cells in the liver. Notably, this transcription reprogramming is also observed in multiple cancer types. Our data demonstrate that epigenetically reprogrammed tissue-specific transcription promotes metastasis and should be targeted therapeutically.

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Tissue-specific transcription reprogramming promotes liver metastasis of colorectal cancer (RNA-Seq)

Project description:Tissue-specific transcription reprogramming promotes liver metastasis of colorectal cancer (RNA-Seq)

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Tissue-specific transcription reprogramming promotes liver metastasis of colorectal cancer.

Project description:Metastasis, the development of secondary malignant growths at a distance from a primary tumor, is the cause of death for 90% of cancer patients, but little is known about how metastatic cancer cells adapt to and colonize new tissue environments. Here, using clinical samples, patient-derived xenograft (PDX) samples, PDX cells, and primary/metastatic cell lines, we discovered that liver metastatic colorectal cancer (CRC) cells lose their colon-specific gene transcription program yet gain a liver-specific gene transcription program. We showed that this transcription reprogramming is driven by a reshaped epigenetic landscape of both typical enhancers and super-enhancers. Further, we identified that the liver-specific transcription factors FOXA2 and HNF1A can bind to the gained enhancers and activate the liver-specific gene transcription, thereby driving CRC liver metastasis. Importantly, similar transcription reprogramming can be observed in multiple cancer types. Our data suggest that reprogrammed tissue-specific transcription promotes metastasis and should be targeted therapeutically.

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Colorectal liver metastases-specific lncRNA CRLM1 inhibits apoptosis and promotes metastasis through transcriptional regulation cooperated with hnRNPK [HNRNPK_OE]

Project description:The survival rate of colorectal liver metastases remains low. Long noncoding lncRNAs is emerging as a novel class of master regulators of cell invasion and metastasis. In this study, analysis of the lncRNA expression dynamics in the colorectal liver metastases, primary colorectal tumor and normal tissues led to the identification of the metastasis-specific expression of a set of lncRNAs including CRLM1. CRLM1 inhibited apoptosis and promoted metastasis and invasion of colorectal cancer cells, and also promoted tumor growth in nude mice. CRLM1 weakly associated with chromatin regions of genes involved in cell adhesion and DNA damage, correlated with CRLM1-regulated gene expression bidirectionally. CRLM1 physically interacts with and promotes the nuclear localization of the metastasis protein hnRNPK. CRLM1 effectively promotes hnRNPK promoter occupancy, and co-regulate gene expression. These findings suggest a potential biomarker and druggable target for treatment of colorectal liver metastases.

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