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Epigenetic profiling of EMT in pancreatic cancer cells (ATAC-seq)

ABSTRACT: Epigenetic profiling of EMT in pancreatic cancer cells (ATAC-seq)

PROVIDER: PRJNA565772 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10126336_1.fastq.gz	Fastqsanger.gz
	SRR10126336_2.fastq.gz	Fastqsanger.gz
	SRR10126337_1.fastq.gz	Fastqsanger.gz
	SRR10126337_2.fastq.gz	Fastqsanger.gz
	SRR10126338_1.fastq.gz	Fastqsanger.gz

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Project description:<p>The involvement of membrane-bound solute carriers (SLCs) in neoplastic transdifferentiation processes is poorly defined. Here, we examined changes in the SLC landscape during epithelial-mesenchymal transition (EMT) of pancreatic cancer cells. We show that two SLCs from the organic anion/cation transporter family, SLC22A10 and SLC22A15, favor EMT via interferon (IFN) α and γ signaling activation of receptor tyrosine kinase-like orphan receptor 1 (ROR1) expression. In addition, SLC22A10 and SLC22A15 allow tumor cell accumulation of glutathione to support EMT via the IFNα/γ-ROR1 axis. Moreover, a pan-SLC22A inhibitor lesinurad reduces EMT-induced metastasis and gemcitabine chemoresistance to prolong survival in mouse models of pancreatic cancer, thus identifying new vulnerabilities for human PDAC.</p>

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