Echanism by which EndoMT in EC produces EVs that may possibly propagate angiostatic effects all through the AT vasculature in obesity. Funding: NIHR15NHLBI, STAT5 drug American Heart AssociationAIREA.ISEV2019 ABSTRACT BOOKSymposium Session 9: EV Biogenesis II Chairs: Bong Hwan Sung; Graca Raposo Place: Level B1, Hall B 17:008:OT09.Unique exosome subtypes have distinct ESCRT-associated biology and control tumour cell adaptation in vivo Shih-Jung Fana, Benjamin Kroegerb, Pauline Mariea, Esther Bridgesa, Kristie McCormicka, John Masona, Helen Sheldona, Claudia Mendesa, Mark Wainwrighta, John Morrisa, Adrian Harrisa, Clive Wilsona and Deborah C I. Goberdhana University of Oxford, Oxford, UK; Melbourne, Australiaa bFunding: This perform was funded by Cancer Investigation UK [C19591/A19076], the CRUK Oxford Centre Improvement Fund [C38302/A12278], BBSRC [BB/ K017462/1, BB/N016300/1, BB/R004862/1], John Fell Fund, Oxford, Wellcome Trust [MICRON; #091911, #107457], Royal College of Surgeons.Peter MacCallum Cancer Centre,OT09.Emerging role of L-type calcium channel-mediated calcium influx in regulating apoptotic bodies formation Thanh Kha Phana, Bo Shib, Niall Geogheganc, Kelly Rogersd and Ivan PooneaIntroduction: Determining the function of certain extracellular vesicle (EV) and exosome subtypes has proved difficult, in element due to the difficulty in untangling the mechanisms leading to their generation. Strategies: We investigated the cell biology behind exosome formation working with the large endosomal compartments provided by an in vivo fly model, and analysis in human HCT116 as well as other cancer cell lines. EV preparations have been also tested in vivo following injection in to human xenografts in mice. We analysed unique EV preparations by mass spectrometry utilizing Tandem Mass Tag labelling to determine alterations in protein cargo of EVs in response to microenvironmental tension. Outcomes: Employing these complementary approaches, we show that microenvironmental anxiety, such as glutamine depletion, leads to a switch in membrane trafficking from the classic late endosomal multivesicular endosomes to Rab11a-positive recycling endosomes and the production of Rab11a-positive exosomes, which promote cell development beneath strain circumstances. This activity is suppressed by blocking ULK1 drug Rab11a-dependent trafficking and ESCRT function. Our proteomics and fly information recommend that some ESCRTs are differentially involved in these two exosome-generating processes. Furthermore, mouse xenografts highlight roles for stress-induced EVs in increasing the turnover of tumour cells, leading to an increase in hypoxic anxiety, linked with choice for aggressive cells that will promote tumour progression. These stress-induced vesicles also have a potent effect on blood vessel growth in vivo. Summary/Conclusion: We conclude that stressinduced EVs and exosomes made in Rab11a-positive recycling endosomes are involved in tumour adaptation.Department of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Bundoora, Australia; bDepartment of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, Australia; cCentre for Dynamic Imaging, Walter and Eliza Hall Institute of Medical Investigation, Melbourne, Australia; d Centre for Dynamic Imaging, Walter and Eliza Hall Institute of Medical Analysis, Melbourne, Australia; eLa Trobe University, Bundoora, AustraliaIntroduction: Dying cells generally break into smaller membrane-bound fragments, known as apoptotic.