Epigenomic reprogramming during pancreatic cancer progression links anabolic glucose metabolism to distant metastasis. Large-scale chondroitin sulfate proteoglycan digestion with chondroitinase gene therapy leads to reduced pathology and modulates macrophage phenotype following spinal cord contusion injury. Neuron-glia interactions in neural plasticity: contributions of neural extracellular matrix and perineuronal nets. The extracellular environment of the CNS: influence on plasticity, sprouting, and axonal regeneration after spinal cord injury. The roles of perineuronal nets and the perinodal extracellular matrix in neuronal function. Genome regulation by polycomb and trithorax: 70 years and counting. Schuettengruber, B., Bourbon, H.-M., Di Croce, L. The epigenetics of tumour initiation: cancer stem cells and their chromatin. Galanin is an autocrine myelin and oligodendrocyte trophic signal induced by leukemia inhibitory factor. ‘Neuro’-peptides in glia: Focus on NPY and galanin. Glutamatergic synaptic input to glioma cells drives brain tumour progression. Loss of p53 drives neuron reprogramming in head and neck cancer. Electrical and synaptic integration of glioma into neural circuits. Nerves in the tumour microenvironment: origin and effects. Role of the nervous system in cancer metastasis.
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Free fatty acids profile among lean, overweight and obese non-alcoholic fatty liver disease patients: a case-control study.
Comprehensive profiling of plasma fatty acid concentrations in young healthy Canadian adults.
Leukemic stem cells evade chemotherapy by metabolic adaptation to an adipose tissue niche. Toward minimal residual disease-directed therapy in melanoma. Tumor metastasis to lymph nodes requires YAP-dependent metabolic adaptation. Targeting metastasis-initiating cells through the fatty acid receptor CD36. A systematic review and meta-analysis of the 2007 WCRF/AICR score in relation to cancer-related health outcomes. Nerve dependence: from regeneration to cancer. The contributions of cancer cell metabolism to metastasis. lipid metabolism at the nexus of diet and tumor microenvironment. In summary, we provide evidence that a dietary metabolite induces stable transcriptional and chromatin changes that lead to a long-term stimulation of metastasis, and that this is related to a proregenerative state of tumour-activated Schwann cells.
Both the PA-induced memory of this proneural signature and its long-term boost in metastasis require the transcription factor EGR2 and the glial-cell-stimulating peptide galanin. Mechanistically, tumour-associated Schwann cells secrete a specialized proregenerative extracellular matrix, the ablation of which inhibits metastasis initiation. Bulk, single-cell and positional RNA-sequencing analyses indicate that genes with this prometastatic memory predominantly relate to a neural signature that stimulates intratumoural Schwann cells and innervation, two parameters that are strongly correlated with metastasis but are aetiologically poorly understood 3, 4.
This PA-induced prometastatic memory requires the fatty acid transporter CD36 and is associated with the stable deposition of histone H3 lysine 4 trimethylation by the methyltransferase Set1A (as part of the COMPASS complex (Set1A/COMPASS)). Tumours from mice that were fed a short-term palm-oil-rich diet (PA), or tumour cells that were briefly exposed to PA in vitro, remained highly metastatic even after being serially transplanted (without further exposure to high levels of PA). Here we show that dietary palmitic acid (PA), but not oleic acid or linoleic acid, promotes metastasis in oral carcinomas and melanoma in mice. Fatty acid uptake and altered metabolism constitute hallmarks of metastasis 1, 2, yet evidence of the underlying biology, as well as whether all dietary fatty acids are prometastatic, is lacking.
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