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Comparing alternative polyadenylation landscapes in highly and poorly metastatic breast cancer cells

ABSTRACT: Comparing alternative polyadenylation landscapes in highly and poorly metastatic breast cancer cells

PROVIDER: PRJNA774893 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16587314.fastq.gz	Fastqsanger.gz
	SRR16587315.fastq.gz	Fastqsanger.gz
	SRR16587316.fastq.gz	Fastqsanger.gz
	SRR16587317.fastq.gz	Fastqsanger.gz
	SRR16587318.fastq.gz	Fastqsanger.gz

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Comparing alternative polyadenylation landscapes in highly and poorly metastatic breast cancer cells

Project description:Cancer cells often co-opt post-transcriptional regulatory mechanisms to achieve pathologic expression of gene networks that drive metastasis. Translational control is a major regulatory hub in oncogenesis, however its effects on cancer progression remain poorly understood. To address this, we used ribosome profiling to compare genome-wide translation efficiencies of poorly and highly metastatic breast cancer cells and patient-derived xenografts. We developed novel regression-based methods to analyze ribosome profiling and alternative polyadenylation data, and identified HNRNPC as a translational controller of a specific mRNA regulon. Mechanistically, HNRNPC, in concert with PABPC4, binds near to poly(A) signals, thereby governing the alternative polyadenylation of a set of mRNAs. We found that HNRNPC and PABPC4 are downregulated in highly metastatic cells, which causes HNRNPC-bound mRNAs to undergo 3’ UTR lengthening and subsequently, translational repression. We showed that modulating HNRNPC expression impacts the metastatic capacity of breast cancer cells in xenograft mouse models. We also found that a small molecule, previously shown to induce a distal-to-proximal poly(A) site switching, counteracts the HNRNPC-PABPC4 driven deregulation of alternative polyadenylation and decreases the metastatic lung colonization by breast cancer cells in vivo.

2023-02-20 | GSE186637 | GEO

Translation efficiency changes measured using ribosome footprinting (Ribo-seq) in poorly and highly metastatic cancer cells

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Poorly metastatic HCT116 vs metastatic E1 colon cancer cell lines

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Gene expression profilling of poorly metastatic MDA cells and highly metastatic LM2 cells

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Gene expression profilling of poorly metastatic MDA cells and highly metastatic LM2 cells.

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Translation efficiency changes measured using ribosome footprinting (Ribo-seq) in poorly and highly metastatic cancer cells

Project description:Translation efficiency changes measured using ribosome footprinting (Ribo-seq) in poorly and highly metastatic cancer cells

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Serum-derived exosomes from mice with highly metastatic breast cancer transfer increased metastatic capacity to a poorly metastatic tumor.

Project description:Altered interaction between CD200 and CD200R represents an example of "checkpoint blockade" disrupting an effective, tumor-directed, host response in murine breast cancer cells. In CD200R1KO mice, long-term cure of EMT6 breast cancer, including metastatic spread to lung and liver, was achieved in BALB/c mice. The reverse was observed with 4THM tumors, an aggressive, inflammatory breast cancer, with increased tumor metastasis in CD200R1KO. We explored possible explanations for this difference. We measured the frequency of circulating tumor cells (CTCs) in peripheral blood of tumor bearers, as well as lung/liver and draining lymph nodes. In some cases mice received infusions of exosomes from nontumor controls, or tumor bearers, with/without additional infusions of anticytokine antibodies. The measured frequency of circulating tumor cells (CTCs) in peripheral blood was equivalent in the two models in WT and CD200R1KO mice. Increased metastasis in EMT6 tumor bearers was seen in vivo following adoptive transfer of serum, or serum-derived exosomes, from 4THM tumor bearers, an effect which was attenuated by anti-IL-6, and anti-IL-17, but not anti-TNFα, antibody. Anti-IL-6 also attenuated enhanced migration of EMT6 cells in vitro induced by 4THM serum or exosomes, or recombinant IL-6. Exosome cytokine proteomic profiles responses in 4THM and EMT6 tumor-bearing mice were regulated by CD200:CD200R interactions, with attenuation of both IL-6 and IL-17 in 4THM CD200(tg) mice, and enhanced levels in 4THM CD200R1KO mice. We suggest these cytokines act on the microenvironment at sites within the host, and/or directly on tumor cells themselves, to increase metastatic potential.

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