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Extracellular matrix interactions provide an escape mechanism for commitment to differentiation in cancer

ABSTRACT: Extracellular matrix interactions provide an escape mechanism for commitment to differentiation in cancer

PROVIDER: PRJNA741247 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14907581.fastq.gz	Fastqsanger.gz
	SRR14907582.fastq.gz	Fastqsanger.gz
	SRR14907583.fastq.gz	Fastqsanger.gz
	SRR14907584.fastq.gz	Fastqsanger.gz
	SRR14907585.fastq.gz	Fastqsanger.gz

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Extracellular matrix interactions provide an escape mechanism for commitment to differentiation in cancer

Project description:We report the new role that the interaction of cells with the surrounding extracellular matrix can exert on the differnetiation patterns controlled by the BMP pathway. In cells bearing Apc mutations, modulation of this pathway triggers cells irresponsive to normal differentiation cues which offers a posible therapeutic anchor for anti-cancer therapies.

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Reconstruction of Extracellular Matrix by Grhl3 Modulates Cell Fate Commitment from Fibroblasts to Induced Cardiomyocytes

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Neural extracellular matrix regulates visual sensory motor integration

Project description:Visual processing depends on sensitive and balanced synaptic neurotransmission. Extracellular matrix proteins in the environment of cells are key modulators in synaptogenesis and synaptic plasticity. In the present study, we provide evidence that the combined loss of the four extracellular matrix components brevican, neurocan, tenascin-C and tenascin-R in quadruple knockout mice leads to severe retinal dysfunction and diminished visual motion processing in vivo. Remarkably, impaired visual motion processing was accompanied by a developmental loss of cholinergic direction-selective starburst amacrine cells. Additionally, we noted imbalance of inhibitory and excitatory synaptic signaling in the quadruple knockout retina. Collectively, the study offers novel insights into the functional importance of four key extracellular matrix proteins for retinal function, visual motion processing and synaptic signaling.

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Extracellular matrix flow guides emergent morphogenesis

Project description:Extracellular matrix flow guides emergent morphogenesis

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Escape from X inactivation in mouse tissues (RNA-Seq)

Project description:X chromosome inactivation (XCI) silences most genes on one X chromosome in female mammals, but some genes escape XCI. To identify escape gene in vivo and to explore molecular mechanisms that regulate this process we analyzed the allele-specific expression and chromatin structure of X-linked genes in mouse tissues and cells with skewed XCI and distinguishable alleles based on single nucleotide polymorphisms. Using a new method to estimate allelic expression, we demonstrate a continuum between complete silencing and significant expression from the inactive X (Xi). Few genes (2-3%) escape XCI to a significant level and only a minority differs between mouse tissues, suggesting stringent silencing and escape controls. Allelic profiles of DNase I hypersensitivity and RNA polymerase II occupancy of genes on the Xi correlate with escape from XCI. Allelic binding profiles of the DNA binding protein CCCTC-binding factor (CTCF) in different cell types indicate that CTCF binding at the promoter correlates with escape. Importantly, CTCF binding at the boundary between escape and silenced domains may prevent the spreading of active escape chromatin into silenced domains. Examination of allelic expression in mouse hybrid tissues.

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Escape from X inactivation in mouse tissues (ChIP-Seq)

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Chemotherapy-induced extracellular matrix remodelling in HGSOC

Project description:Chemotherapy-induced extracellular matrix remodelling in HGSOC

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Defining the effect of extracellular matrix on cellular identity

Project description:Intestinal epithelial cells from the small intestine were seeded in either Matrigel or purified Type I Collagen in order to define the effect of matrix on cell fate.

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Project description:Extracellular matrix interactions play essential roles in normal physiology and many pathological processes. Here, we report a novel screening platform capable of measuring phenotypic responses to combinations of ECM molecules. While the importance of ECM interactions in metastasis is well documented, systematic approaches to identify their roles in distinct stages of tumorigenesis have not been described. Using a genetic mouse model of lung adenocarcinoma, we measured the ECM-dependent adhesion of tumor-derived cells. Hierarchical clustering of adhesion profiles generated using this platform differentially segregated metastatic cell lines from primary tumor lines. Furthermore, we uncovered that metastatic cells selectively associate with fibronectin when in combination with galectin-3, galectin-8, or laminin. These interactions appear to be mediated in part by Î±3Î²1 integrin both in vitro and in vivo. We show that these galectins also correlate with human disease at both a transcriptional and histological level. Thus, our in vitro platform allowed us to interrogate the interactions of metastatic cells with their surrounding environment, and identified ECM and integrin interactions that could lead to therapeutic targets for metastasis prevention. Cell lines derived from murine lung primary adenocarcinomas and their metastases (Winslow et al., 2011 Nature 473:101-104)

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