Extracellular Vesicles Shedding Promotes Melanoma Growth in Response to Chemotherapy
Carregando...
Citações na Scopus
28
Tipo de produção
article
Data de publicação
2019
Título da Revista
ISSN da Revista
Título do Volume
Editora
NATURE PUBLISHING GROUP
Citação
SCIENTIFIC REPORTS, v.9, article ID 14482, 12p, 2019
Resumo
Extracellular vesicles (EVs) are emerging as key players in intercellular communication. EVs can transfer biological macromolecules to recipient cells, modulating various physiological and pathological processes. It has been shown that tumor cells secrete large amounts of EVs that can be taken up by malignant and stromal cells, dictating tumor progression. In this study, we investigated whether EVs secreted by melanoma cells in response to chemotherapy modulate tumor response to alkylating drugs. Our findings showed that human and murine melanoma cells secrete more EVs after treatment with temozolomide and cisplatin. We observed that EVs shed by melanoma cells after temozolomide treatment modify macrophage phenotype by skewing macrophage activation towards the M2 phenotype through upregulation of M2-marker genes. Moreover, these EVs were able to favor melanoma re-growth in vivo, which was accompanied by an increase in Arginase 1 and IL10 gene expression levels by stromal cells and an increase in genes related to DNA repair, cell survival and stemness in tumor cells. Taken together, this study suggests that EVs shed by tumor cells in response to chemotherapy promote tumor repopulation and treatment failure through cellular reprogramming in melanoma cells.
Palavras-chave
Referências
- Abels ER, 2016, CELL MOL NEUROBIOL, V36, P301, DOI 10.1007/s10571-016-0366-z
- Al-Nedawi K, 2008, NAT CELL BIOL, V10, P619, DOI 10.1038/ncb1725
- Ayob AZ, 2018, J BIOMED SCI, V25, DOI 10.1186/s12929-018-0426-4
- Baj-Krzyworzeka M, 2016, J TRANSL MED, V14, DOI 10.1186/s12967-016-0789-9
- Bardi GT, 2018, CYTOKINE, V105, P63, DOI 10.1016/j.cyto.2018.02.002
- Becker A, 2016, CANCER CELL, V30, P836, DOI 10.1016/j.ccell.2016.10.009
- Begicevic RR, 2017, INT J MOL SCI, V18, DOI 10.3390/ijms18112362
- Chang JM, 2019, FASEB J, V33, P114, DOI 10.1096/fj.201800019RR
- Chow A, 2014, SCI REP-UK, V4, DOI 10.1038/srep05750
- Corcoran C, 2012, PLOS ONE, V7, DOI 10.1371/journal.pone.0050999
- Costa-Silva B, 2015, NAT CELL BIOL, V17, P816, DOI 10.1038/ncb3169
- de Vrij J, 2015, INT J CANCER, V137, P1630, DOI 10.1002/ijc.29521
- Desrochers LM, 2016, DEV CELL, V37, P301, DOI 10.1016/j.devcel.2016.04.019
- El-Khattouti A, 2014, CANCER LETT, V343, P123, DOI 10.1016/j.canlet.2013.09.024
- Eton O, 2002, J CLIN ONCOL, V20, P2045, DOI 10.1200/JCO.2002.07.044
- Feng QY, 2017, NAT COMMUN, V8, DOI 10.1038/ncomms14450
- Hong BS, 2009, BMC GENOMICS, V10, DOI 10.1186/1471-2164-10-556
- Huang Z, 2017, ONCOL RES, V25, P651, DOI 10.3727/096504016X14752792816791
- Ji ZY, 2015, J INVEST DERMATOL, V135, P1863, DOI 10.1038/jid.2015.105
- Jung T, 2009, NEOPLASIA, V11, P1093, DOI 10.1593/neo.09822
- Ke XQ, 2017, NEOPLASIA, V19, P941, DOI 10.1016/j.neo.2017.06.007
- Keklikoglou I, 2019, NAT CELL BIOL, V21, P190, DOI 10.1038/s41556-018-0256-3
- Khayat D, 2002, J CLIN ONCOL, V20, P2411, DOI 10.1200/JCO.2002.20.10.2411
- King HW, 2012, BMC CANCER, V12, DOI 10.1186/1471-2407-12-421
- Kreger BT, 2016, CANCERS, V8, DOI 10.3390/cancers8120111
- Li YQ, 2012, CANCER RES, V72, P576, DOI 10.1158/0008-5472.CAN-11-3070
- Livak KJ, 2001, METHODS, V25, P402, DOI 10.1006/meth.2001.1262
- Logozzi M, 2017, CANCER LETT, V403, P318, DOI 10.1016/j.canlet.2017.06.036
- Lundholm M, 2014, PLOS ONE, V9, DOI 10.1371/journal.pone.0108925
- Lv LH, 2012, J BIOL CHEM, V287, P15874, DOI 10.1074/jbc.M112.340588
- Lv MM, 2014, TUMOR BIOL, V35, P10773, DOI 10.1007/s13277-014-2377-z
- Matsumoto A, 2017, CANCER SCI, V108, P1803, DOI 10.1111/cas.13310
- Mattia G, 2018, CELL DEATH DIS, V9, DOI 10.1038/s41419-017-0059-7
- Nazarenko I, 2010, CANCER RES, V70, P1668, DOI 10.1158/0008-5472.CAN-09-2470
- Noy R, 2014, IMMUNITY, V41, P49, DOI 10.1016/j.immuni.2014.06.010
- Parolini I, 2009, J BIOL CHEM, V284, P34211, DOI 10.1074/jbc.M109.041152
- Peinado H, 2012, NAT MED, V18, P883, DOI 10.1038/nm.2753
- Phadke MS, 2015, MOL CANCER THER, V14, P1354, DOI 10.1158/1535-7163.MCT-14-0832
- Piao Yin Ji, 2018, Oncotarget, V9, P7398, DOI 10.18632/oncotarget.23238
- Qu L, 2016, CANCER CELL, V29, P653, DOI 10.1016/j.ccell.2016.03.004
- Samuel P., 2018, PHILOS T R SOC LON B, V373, P1737
- Shimoda M, 2017, BBA-MOL CELL RES, V1864, P1989, DOI 10.1016/j.bbamcr.2017.05.027
- Shinohara H, 2017, J IMMUNOL, V199, P1505, DOI 10.4049/jimmunol.1700167
- Tian H, 2015, CANCER LETT, V358, P8, DOI 10.1016/j.canlet.2014.12.038
- van Schaijik B, 2018, J CLIN PATHOL, V71, P88, DOI 10.1136/jclinpath-2017-204815
- Vella LJ, 2017, NEOPLASIA, V19, P932, DOI 10.1016/j.neo.2017.07.002
- Wendler F, 2017, ONCOGENE, V36, P877, DOI 10.1038/onc.2016.253
- Wouters J, 2013, PLOS ONE, V8, DOI 10.1371/journal.pone.0076550
- Wu LJ, 2016, TUMOR BIOL, V37, P12169, DOI 10.1007/s13277-016-5071-5
- Wysoczynski M, 2009, INT J CANCER, V125, P1595, DOI 10.1002/ijc.24479
- Xiao X, 2014, PLOS ONE, V9, DOI 10.1371/journal.pone.0089534
- Yanez-Mo M, 2015, J EXTRACELL VESICLES, V4, DOI 10.3402/jev.v4.27066
- Ye SB, 2016, J PATHOL, V240, P329, DOI 10.1002/path.4781
- Ye SB, 2014, ONCOTARGET, V5, P5439, DOI 10.18632/oncotarget.2118
- Zeng AL, 2017, ONCOGENE, V36, P5369, DOI 10.1038/onc.2017.134
- Zhang HY, 2016, CANCER LETT, V375, P331, DOI 10.1016/j.canlet.2016.03.026
- Zhang HC, 2012, STEM CELLS DEV, V21, P3289, DOI 10.1089/scd.2012.0095