MassIVE MSV000097473

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GNPS - Metabolic adaptations of micrometastases alter EV production to generate invasive microenvironments

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Description

Altered cellular metabolism has been associated with acquisition of invasive phenotypes during metastasis. To study this, we combined a genetically engineered mouse model of mammary carcinoma with syngeneic transplantation and primary tumour resection to generate isogenic cells from primary tumours and their corresponding lung micrometastases. Metabolic analyses indicated that micrometastatic cells increase proline production at the expense of glutathione synthesis leading to a reduction in total glutathione levels. Micrometastatic cells also have altered sphingomyelin metabolism leading to increased intracellular levels of specific ceramides. The combination of these two metabolic adaptations alters small extracellular vesicle (sEV) production to drive generation of an invasive microenvironment. Indeed, micrometastatic cells shut-down Rab27-dependent production of sEVs and, instead, switch-on neutral sphingomyelinase-2 (nSM2)- dependent sEV release. sEVs released in a nSM2-dependent manner from micrometastatic cells, in turn, influence the ability of fibroblasts to deposit extracellular matrix which promotes cancer cell invasiveness. These data provide evidence that metabolic rewiring drives invasive processes in metastasis by influencing sEV release [doi:10.25345/C59S1KX93] [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: metabolism ; extracellular vesicles (EVs) ; invasiveness ; micrometastases ; mammary cancer ; DatasetType:Metabolomics

Contact

Principal Investigators:
(in alphabetical order) 		Cassie Clarke, CRUK Scotland Institute, United Kingdom
David Sumpton, CRUK Scotland Insititue, United Kingdom
Jim Norman, CRUK Scotland Institute, United Kingdom
Michalis Gounis, Turku Centre for Biotechnology, Finland
Submitting User: dsumpton
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GNPS content goes here (MSV000097473 [task=0078c09d79764a7499516344ae75954d])
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