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We welcome you to read up on some recent hypoxic research being conducted using a Whitley Hypoxystation.
Cancer EV stimulate endothelial glycolysis to fuel protein synthesis via mTOR and AMPKα activation.
Author: Beaumont et al (2024)
Topic: Investigating how cancer cell extracellular vesicles (EV) regulate cellular metabolism and protein synthesis.
Five point summary:
- Cancer cells excrete exosomes and microvesicles to facilitate intercellular communication with surrounding cells to create an growth promoting environment.
- HT29, U87, MDA-MB-231, EC-RF-24, HMEC-1, MRC5, U937 and BJ cells were cultured in supplemented DMEM + 10% foetal bovine serum.
- Cells were exposed to normoxic atmospheric conditions and 2 levels of hypoxic atmospheric conditions: 0.2% oxygen in a Whitley H85 Hypoxystation and 0.02% oxygen in a Whitley A35 Anaerobic Workstation.
- EV were extracted using centrifugation and size exclusion chromatography and were characterised using MISEV2023 guidelines to ensure any observations could be attributed to a pure EV isolate rather than co-isolated contaminants.
- Cancer cell-derived EV contain glycolytic enzymes, including pyruvate kinase PKM, L-lactate dehydrogenase and glyceraldehyde-3-phosphate dehydrogenase, and transfer cargo to respective organelles as well as increasing glucose metabolism in recipient cells.
Hypoxia Insights:
- Hypoxic cancer cell derived EV stimulate glucose uptake in endothelial cells to fuel amino acid synthesis and stimulate amino acid uptake to increase protein synthesis and regulate cellular metabolism and protein synthesis in acceptor cells through increased activation of mTOR and AMPKα.
- The effects of EV on recipient cells is dependent on cancer cellular type rather than oxygenation.
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