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Death Receptor 5 Displayed on Extracellular Vesicles Decreases University of Groningen Death Receptor 5 Displayed on Extracellular Vesicles Decreases TRAIL Sensitivity of Colon Cancer Cells Setroikromo, Rita; Zhang, Baojie; Reis, Carlos R; Mistry, Rima H; Quax, Wim J Published in: Frontiers in Cell and Developmental Biology DOI: 10.3389/fcell.2020.00318 IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from it. Please check the document version below. Document Version Publisher's PDF, also known as Version of record Publication date: 2020 Link to publication in University of Groningen/UMCG research database Citation for published version (APA): Setroikromo, R., Zhang, B., Reis, C. R., Mistry, R. H., & Quax, W. J. (2020). Death Receptor 5 Displayed on Extracellular Vesicles Decreases TRAIL Sensitivity of Colon Cancer Cells. Frontiers in Cell and Developmental Biology, 8, 318. [318]. https://doi.org/10.3389/fcell.2020.00318 Copyright Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons). The publication may also be distributed here under the terms of Article 25fa of the Dutch Copyright Act, indicated by the “Taverne” license. More information can be found on the University of Groningen website: https://www.rug.nl/library/open-access/self-archiving-pure/taverne- amendment. Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum. fcell-08-00318 May 15, 2020 Time: 17:18 # 1 ORIGINAL RESEARCH published: 19 May 2020 doi: 10.3389/fcell.2020.00318 Death Receptor 5 Displayed on Extracellular Vesicles Decreases TRAIL Sensitivity of Colon Cancer Cells Rita Setroikromo†, Baojie Zhang†, Carlos R. Reis, Rima H. Mistry and Wim J. Quax* Department of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy, University of Groningen, Groningen, Netherlands Tumor necrosis factor–related apoptosis inducing ligand (TRAIL) is considered to be a promising antitumor drug because of its selective proapoptotic properties on tumor cells. However, the clinical application of TRAIL is until now limited because of the resistance of several cancer cells, which can occur at various levels in the TRAIL signaling pathway. The role of decoy receptors that can side-track TRAIL, thereby Edited by: Olivier Micheau, preventing the formation of an activated death receptor, has been extensively studied. In Université de Bourgogne, France this study, we have focused on extracellular vesicles (EVs) that are known to play a role Reviewed by: in cell-to-cell communication and that can be released by donor cells into the medium Marine Eduard Gasparian, Institute of Bioorganic Chemistry transferring their components to recipient cells. TRAIL-induced apoptotic signaling is (RAS), Russia triggered upon the binding of two death receptors, DR4 and DR5. Here, we found Ladislav Andera, that DR5 but not DR4 is present in the conditioned medium (CM)–derived from various Institute of Molecular Genetics (ASCR), Czechia cancer cells. Moreover, we observed that DR5 was exposed on EVs and can act as *Correspondence: “decoy receptor” for binding to TRAIL. This results in a strongly reduced number of Wim J. Quax apoptotic cells upon treatment with DR5-specific TRAIL variant DHER in CM. This [email protected] reduction happened with EVs containing either the long or short isoform of DR5. Taken †These authors have contributed equally to this work together, we demonstrated that colon rectal tumor cells can secrete DR5-coated EVs, and this can cause TRAIL resistance. This is to our knowledge a novel finding and Specialty section: provides new insights into understanding TRAIL sensitivity. This article was submitted to Signaling, Keywords: extracellular vesicles, DR5, TRAIL, apoptosis, conditioned medium, receptor–ligand trafficking a section of the journal Frontiers in Cell and Developmental Biology INTRODUCTION Received: 24 January 2020 Accepted: 09 April 2020 The secretion of extracellular vesicles (EVs) is an evolutionally conserved process spanning Published: 19 May 2020 from bacteria to humans and plants (Rivera et al., 2010; Van Niel et al., 2018; Cui et al., Citation: 2019). The significance of EVs on the one hand relates to their capacity to eliminate unwanted Setroikromo R, Zhang B, Reis CR, components from the cell and on the other hand to their capability to communicate with Mistry RH and Quax WJ (2020) Death other cells by exchanging components–from DNA to protein–and thereby influencing the signal Receptor 5 Displayed on Extracellular Vesicles Decreases TRAIL Sensitivity transduction pathways of target cells (Colombo et al., 2014; Yáñez-Mó et al., 2015). They are of Colon Cancer Cells. highly heterogeneous and can be broadly divided into two main categories based on their Front. Cell Dev. Biol. 8:318. biogenesis and characterizations (Colombo et al., 2014; Van Niel et al., 2018). The term exosomes doi: 10.3389/fcell.2020.00318 (30–100 nm) was first used to describe the EVs released by reticulocytes during differentiation Frontiers in Cell and Developmental Biology| www.frontiersin.org 1 May 2020| Volume 8| Article 318 fcell-08-00318 May 15, 2020 Time: 17:18 # 2 Setroikromo et al. DR5-Coated Vesicles as Decoy Receptors (Johnstone et al., 1987). It originates from inward budding of MATERIALS AND METHODS endosome membrane creating the so-called cargo-containing intraluminal vesicle (ILV) inside the early endosome. These Cell Lines and Culture Conditions early endosomes can either be directed to the lysosomes or Human colorectal carcinoma cell lines (Colo205, HCT 116, fused together and mature to the late multivesicular endosomes and DLD-1), human Burkitt lymphoma B cell line (BJAB), (MVEs). MVEs when fused with cell membrane can release and the Chinese hamster ovary cell line (CHO) were cultured their cargo-containing ILV in the extracellular space, and these in RPMI1640 medium supplemented with 10% fetal bovine small vesicles are called exosomes (McGough and Vincent, serum, 100 U/mL penicillin, and 100 mg/mL streptomycin in 2016). The other group of EVs is named microvesicles (50– ◦ a humidified incubator at 37 C with 5% CO2. All materials 1,000 nm, up to 10 mm), which are directly formed after budding mentioned above were purchased from Thermo Fisher Scientific or fission of plasma membrane in response to diverse cell (Waltham, MA, United States). BJAB cell lines, the wild-type cells stimulation; this includes the apoptotic bodies. Owing to their BJAB (BJAB WT), BJAB overexpressing DR5 (BJAB DR5), and varied compositions, increasing evidence shows that EVs act as a deficient DR5 short isoform (BJAB DR5s DEF) were kindly signaling vesicles not only in normal cell homeostasis but also in provided by Dr. Andrew Thornburn (University of Colorado many pathological conditions (Cocucci et al., 2009). Health Sciences Centre, Aurora, CO, United States). CHO cell Cancer is a diverse group of diseases caused by proliferating lines, the wild-type cells (CHO WT), a mutant overexpressing cells traditionally treated with chemotherapy and/or DR5 long isoform (CHO TV1), and a mutant overexpressing radiotherapy. These, however, also give harmful side effects to DR5 short isoform (CHO TV2) were provided by Organon healthy cells. More preferred therapeutics are being developed in (Oss, Netherlands). such a way that they selectively target cancer cells and treatment with tumor necrosis factor–related apoptosis inducing ligand Reagents (TRAIL) is considered to be promising because of its naturally Soluble (aa 114–281) wild-type TRAIL (TRAIL WT), DR4- proapoptotic properties specifically directed to cancer cells specific TRAIL variant (4C7), and DR5-specific TRAIL variant (Wong et al., 2019). Binding of TRAIL to two death receptors (DHER) were constructed and produced as previously described (DR4 and DR5) triggers the recruitment of Fas-associated (Van Der Sloot et al., 2006; Reis et al., 2010). death domain and subsequent pro–caspase-8. This complex, also known as death-inducing signaling complex (DISC), will Collecting Conditioned Medium and initiate downstream caspase-dependent apoptotic signaling and eventually leads to cell death (Nagata, 1997). Although cancer Isolation of EVs cells are more prone to TRAIL-induced cell death than normal Cells were cultured at the concentration of 150,000 cells/mL in exosome-free medium for 48 h in humidified incubator cells, this signaling pathway can be interrupted by many other ◦ factors that lead to resistance in several cancer cells. For instance, at 37 C with 5% carbon dioxide. Medium was collected and three decoy receptors (DcR1, DcR2, and OPG) can also bind spun down at 250 g for 10 min to discard the floating cells. to TRAIL and thereby decrease the availability of free TRAIL This supernatant is from now on called conditioned medium for the binding to the death receptors, leading to inhibition of (CM). EVs were isolated by differential centrifugation strategy: apoptosis (Mahalingam et al., 2009). Despite the importance first, sedimentation of CM at 3,000 g for 15 min; second, of this classical ligand–receptor binding to induce apoptosis, sedimentation of the supernatant at 17,000 g for 20 min; and ligand-induced receptor internalization, and/or intercellular finally with ultracentrifugation at 30,000 g for 3 h. From the last run, the pellet was used as EVs and resuspended in phosphate- receptor trafficking are also important for adequate transduction ◦ of the apoptosis signaling. Likewise, nuclear localization of buffered saline (PBS) and stored at −80 C. DR5 by importin b1 decreases TRAIL-induced cell death in human tumor cells (Kojima et al., 2011).
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