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ABSTRACT: Cell migration

PROVIDER: PRJNA431595 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6511570.fastq.gz	Fastqsanger.gz
	SRR6511580.fastq.gz	Fastqsanger.gz
	SRR6511571.fastq.gz	Fastqsanger.gz
	SRR6511581.fastq.gz	Fastqsanger.gz
	SRR6511572.fastq.gz	Fastqsanger.gz

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Project description:This 121-node Boolean regulatory network model that synthesizes mechanosensitive signaling that links anchorage and matrix stiffness to proliferation and migration, and cell density to contact inhibition. It can reproduce anchorage dependence and anoikis, detachment-induced cytokinesis errors, the effect of matrix stiffness on proliferation, and contact inhibition of proliferation and migration by two mechanisms that converge on the YAP transcription factor. In addition, this model offers testable predictions related to cell cycle-dependent sensitivity to anoikis, the molecular requirements for abolishing contact inhibition, substrate stiffness-dependent expression of the catalytic subunit of PI3K, heterogeneity of migratory and non-migratory phenotypes in sub-confluent monolayers, and linked inhibition but semi-independent induction of proliferation versus migration as a function of cell density and mitogenic stimulation. The model is an extended version of the growth signaling, cell cycle and apoptosis model published in Sizek et al, PLoS Comp. Biol. 15(3): e1006402, 2019.

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Project description:Energy metabolism is highly interdependent with adaptive cell migration in vivo. Mechanical confinement is a critical physical cue that induces switchable migration modes of the mesenchymal-to-amoeboid transition (MAT). However, the energy states in distinct migration modes, especially amoeboid-like stable bleb (A2) movement, remain unclear. In this report, we developed multivalent DNA framework-based nanomachines to explore strategical mitochondrial trafficking and differential ATP levels during cell migration in mechanically heterogeneous microenvironments. Through single-particle tracking and metabolomic analysis, we revealed that fast A2-moving cells driven by biomimetic confinement recruited back-end positioning of mitochondria for powering highly polarized cytoskeletal networks, preferentially adopting an energy-saving mode compared with a mesenchymal mode of cell migration. We present a versatile DNA nanotool for cellular energy exploration and highlight that adaptive energy strategies coordinately support switchable migration modes for facilitating efficient metastatic escape, offering a new perspective for therapeutic interventions in cancer metastasis.

2024-03-25 | MTBLS9657 | MetaboLights

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Effect of Neoadjuvant Radiation on Tumor Infiltrating T-cells by Low Dose Radiation in Colorectal Liver Metastases

Project description:The efficiency of T cell based immunotherapies is affected by the insufficient migration and activity of tumor specific effector T cells in the tumor. Aim of this phase I/II clinical trial is to evaluate whether a neoadjuvant, low dose radiotherapy can improve T cell connected anti tumor immune response in colorectal liver metastases. The primary endpoint is the number of tumor infiltrating T cells. Furthermore the T cell activity in situ, the number of regulatory T cells and the frequency of tumor reactive T cells in the blood and bone marrow will be examined.

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Project description:Hepatocellular carcinoma (HCC), a prevalent malignant neoplasm, presents significant therapeutic challenges. However, the key factors and mechanisms driving HCC metastasis remain incompletely understood. This study aimed to elucidate the mechanism through which CHML regulates the migration and invasion of HCC cells. Following CHML knockout or overexpression, we assessed the proliferative capacity of HCC cells using the Cell Counting Kit-8 (CCK-8) assay, 5-ethynyl-2′-deoxyuridine (EdU) incorporation, colony formation assay, and subcutaneous xenograft tumor models in nude mice. Cell migration and invasion were evaluated using wound healing and Transwell assays. Results demonstrated that CHML knockout significantly inhibited the migration and invasion of HCC cells in vitro, whereas CHML overexpression promoted these phenotypes. Transcriptomic sequencing revealed CHML-mediated regulation of migration-associated pathways, whereas untargeted metabolomics identified choline metabolism as a key significantly altered pathway. Notably, the integration of transcriptomics and untargeted metabolomics identified choline metabolism as a pivotal pathway in CHML-regulated migration and invasion. The subsequent mechanistic analysis demonstrated that CHML upregulated the Solute carrier family 44 member 3 (SLC44A3) to enhance choline uptake, thereby increasing phosphatidic acid (PA) production. This metabolic shift activated MAPK and PI3K-AKT signaling cascades, ultimately driving HCC cell migration and invasion. Our findings provide novel insights into metabolic dependencies in HCC metastasis and position CHML as a promising therapeutic target.

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