Combined p14ARF and Interferon-beta Gene Transfer to the Human Melanoma Cell Line SK-MEL-147 Promotes Oncolysis and Immune Activation

Imagem de Miniatura
Arquivos
art_CERQUEIRA_Combined_p14ARF_and_Interferonbeta_Gene_Transfer_to_the_2020.PDF (1.61 MB)
Citações na Scopus
5
Tipo de produção
article
Data de publicação
2020
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
FRONTIERS MEDIA SA
Autores
CLAVIJO-SALOMON, Maria Alejandra
CARDOSO, Elaine Cristina
Citação
FRONTIERS IN IMMUNOLOGY, v.11, article ID 576658, 13p, 2020
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Immune evasion is an important cancer hallmark and the understanding of its mechanisms has generated successful therapeutic approaches. Induction of immunogenic cell death (ICD) is expected to attract immune cell populations that promote innate and adaptive immune responses. Here, we present a critical advance for our adenovirus-mediated gene therapy approach, where the combined p14ARF and human interferon-beta (IFN beta) gene transfer to human melanoma cells led to oncolysis, ICD and subsequent activation of immune cells. Our results indicate that IFN beta alone or in combination with p14ARF was able to induce massive cell death in the human melanoma cell line SK-MEL-147, though caspase 3/7 activation was not essential. In situ gene therapy of s.c. SK-MEL-147 tumors in Nod-Scid mice revealed inhibition of tumor growth and increased survival in response to IFN beta alone or in combination with p14ARF. Emission of critical markers of ICD (exposition of calreticulin, secretion of ATP and IFN beta) was stronger when cells were treated with combined p14ARF and IFN beta gene transfer. Co-culture of previously transduced SK-MEL-147 cells with monocyte-derived dendritic cells (Mo-DCs) derived from healthy donors resulted in increased levels of activation markers HLA-DR, CD80, and CD86. Activated Mo-DCs were able to prime autologous and allogeneic T cells, resulting in increased secretion of IFN gamma, TNF-alpha, and IL-10. Preliminary data showed that T cells primed by Mo-DCs activated with p14ARF+IFN beta-transduced SK-MEL-147 cells were able to induce the loss of viability of fresh non-transduced SK-MEL-147 cells, suggesting the induction of a specific cytotoxic population that recognized and killed SK-MEL-147 cells. Collectively, our results indicate that p14ARF and IFN beta delivered by our adenoviral system induced oncolysis in human melanoma cells accompanied by adaptive immune response activation and regulation.
Palavras-chave
melanoma, adenovirus (Ad) vector, oncolysis, immunogenic cell death (ICD), immunotherapy
URI
https://observatorio.fm.usp.br/handle/OPI/38524
Referências
  1. ALISON MR, 1992, J ROY COLL PHYS LOND, V26, P25
  2. Balch CM, 2001, J CLIN ONCOL, V19, P3635, DOI 10.1200/JCO.2001.19.16.3635
  3. Cechim G, 2019, AN ACAD BRAS CIENC, V91, DOI 10.1590/0001-3765201920190310
  4. Cerqueira OLD, 2015, ONCOTARGET, V6, P9397, DOI 10.18632/oncotarget.3351
  5. Choi AH, 2016, BIOMEDICINES, V4, DOI 10.3390/biomedicines4030018
  6. David TIP, 2020, SCI REP-UK, V10, DOI 10.1038/s41598-020-74826-y
  7. Davola ME, 2019, ONCOIMMUNOLOGY, V8, DOI 10.1080/2162402X.2019.1596006
  8. de Matos AL, 2020, MOL THER-METH CLIN D, V17, P349, DOI 10.1016/j.omtm.2020.01.001
  9. Dieckmann D, 2005, INT IMMUNOL, V17, P621, DOI 10.1093/intimm/dxh243
  10. Elliott MR, 2009, NATURE, V461, P282, DOI 10.1038/nature08296
  11. Filley AC, 2017, FRONT ONCOL, V7, DOI 10.3389/fonc.2017.00106
  12. FOUNTAIN JW, 1992, P NATL ACAD SCI USA, V89, P10557, DOI 10.1073/pnas.89.21.10557
  13. Fukuhara H, 2016, CANCER SCI, V107, P1373, DOI 10.1111/cas.13027
  14. Galluzzi L, 2020, J IMMUNOTHER CANCER, V8, DOI [10.1136/jitc-2019-000337corr1, 10.1136/jitc-2019-000337]
  15. Galluzzi L, 2018, CELL DEATH DIFFER, V25, P486, DOI 10.1038/s41418-017-0012-4
  16. Giglia-Mari G, 2003, HUM MUTAT, V21, P217, DOI 10.1002/humu.10179
  17. Green DR, 2016, CELL DEATH DIFFER, V23, P915, DOI 10.1038/cdd.2015.172
  18. Gros A, 2016, NAT MED, V22, P433, DOI 10.1038/nm.4051
  19. Gujar S, 2018, TRENDS IMMUNOL, V39, P209, DOI 10.1016/j.it.2017.11.006
  20. Haanen JBAG, 2017, CELL, V170, P1055, DOI 10.1016/j.cell.2017.08.031
  21. Hansel A, 2011, J ALLERGY CLIN IMMUN, V127, P787, DOI 10.1016/j.jaci.2010.12.009
  22. Hanahan D, 2011, CELL, V144, P646, DOI 10.1016/j.cell.2011.02.013
  23. Huang Q, 2011, NAT MED, V17, P860, DOI 10.1038/nm.2385
  24. Hunger A, 2017, CELL DEATH DIS, V8, DOI 10.1038/cddis.2017.201
  25. Hunger A, 2017, CELL DEATH DISCOV, V3, DOI 10.1038/cddiscovery.2017.17
  26. Idzko M, 2002, BLOOD, V100, P925, DOI 10.1182/blood.V100.3.925
  27. Ito Y, 2001, J CLIN APHERESIS, V16, P186, DOI 10.1002/jca.1032
  28. JAMES CD, 1991, CANCER RES, V51, P1684
  29. Kaufman HL, 2015, NAT REV DRUG DISCOV, V14, P642, DOI 10.1038/nrd4663
  30. Kaufmann SH, 2000, EXP CELL RES, V256, P42, DOI 10.1006/excr.2000.4838
  31. Kemp RA, 2001, J IMMUNOL, V167, P6497, DOI 10.4049/jimmunol.167.11.6497
  32. Kroemer G, 2013, ANNU REV IMMUNOL, V31, P51, DOI 10.1146/annurev-immunol-032712-100008
  33. Li F, 2010, SIAM J IMAGING SCI, V3, P1, DOI 10.1137/090748421
  34. Lomas A, 2012, BRIT J DERMATOL, V166, P1069, DOI 10.1111/j.1365-2133.2012.10830.x
  35. Lundberg K, 2014, IMMUNOLOGY, V142, P279, DOI 10.1111/imm.12252
  36. Ma Y, 2013, IMMUNITY, V38, P729, DOI 10.1016/j.immuni.2013.03.003
  37. Marelli G, 2018, FRONT IMMUNOL, V9, DOI 10.3389/fimmu.2018.00866
  38. Medrano RFV, 2017, ONCOTARGET, V8, P71249, DOI 10.18632/oncotarget.19531
  39. Merkel CA, 2013, CANCER GENE THER, V20, P317, DOI 10.1038/cgt.2013.23
  40. Merkel CA, 2010, BMC CANCER, V10, DOI 10.1186/1471-2407-10-316
  41. MIYAKOSHI J, 1990, CANCER RES, V50, P278
  42. Mizuguchi H, 2001, GENE THER, V8, P730, DOI 10.1038/sj.gt.3301453
  43. Naing A, 2018, CANCER CELL, V34, P775, DOI 10.1016/j.ccell.2018.10.007
  44. Obeid M, 2007, NAT MED, V13, P54, DOI 10.1038/nm1523
  45. Oleinika K, 2013, CLIN EXP IMMUNOL, V171, P36, DOI 10.1111/j.1365-2249.2012.04657.x
  46. Panaretakis T, 2009, EMBO J, V28, P578, DOI 10.1038/emboj.2009.1
  47. Peng HH, 2006, ANAL BIOCHEM, V354, P140, DOI 10.1016/j.ab.2006.04.032
  48. Catani JPP, 2016, TRANSL ONCOL, V9, P565, DOI 10.1016/j.tranon.2016.09.011
  49. Qin XQ, 2001, MOL THER, V4, P356, DOI 10.1006/mthe.2001.0464
  50. Ricci MS, 2006, ONCOLOGIST, V11, P342, DOI 10.1634/theoncologist.11-4-342
  51. SALLUSTO F, 1994, J EXP MED, V179, P1109, DOI 10.1084/jem.179.4.1109
  52. Sanchez NS, 2017, PHARMACOGENOMICS, V18, P1525, DOI 10.2217/pgs-2017-0094
  53. Sandoval R, 2004, J BIOL CHEM, V279, P32275, DOI 10.1074/jbc.M313830200
  54. Schreiber RD, 2011, SCIENCE, V331, P1565, DOI 10.1126/science.1203486
  55. Sharpless NE, 2003, ONCOGENE, V22, P3092, DOI 10.1038/sj.onc.1206461
  56. Shirley JL, 2020, MOL THER, V28, P709, DOI 10.1016/j.ymthe.2020.01.001
  57. Simmons DP, 2012, J IMMUNOL, V188, P3116, DOI 10.4049/jimmunol.1101313
  58. Steffensen MA, 2013, J VIROL, V87, P6283, DOI 10.1128/JVI.00465-13
  59. Strauss BE, 2018, CLINICS, V73, DOI 10.6061/clinics/2018/e479s
  60. Strebhardt K, 2008, NAT REV CANCER, V8, P473, DOI 10.1038/nrc2394
  61. Takaoka A, 2003, NATURE, V424, P516, DOI 10.1038/nature01850
  62. Tamura RE, 2020, GENE THER, V27, P15, DOI 10.1038/s41434-019-0071-x
  63. Tamura RE, 2017, HUM GENE THER, V28, P639, DOI 10.1089/hum.2016.139
  64. TOMAYKO MM, 1989, CANCER CHEMOTH PHARM, V24, P148, DOI 10.1007/BF00300234
  65. Vaha-Koskela MJV, 2007, CANCER LETT, V254, P178, DOI 10.1016/j.canlet.2007.02.002
  66. Medrano RFV, 2016, CANCER IMMUNOL IMMUN, V65, P371, DOI 10.1007/s00262-016-1807-8
  67. Villani AC, 2017, SCIENCE, V356, DOI 10.1126/science.aah4573
  68. Wemeau M, 2010, CELL DEATH DIS, V1, DOI 10.1038/cddis.2010.82
  69. Zitvogel L, 2010, CLIN CANCER RES, V16, P3100, DOI 10.1158/1078-0432.CCR-09-2891

Coleções
Artigos e Materiais de Revistas Científicas - HC/ICESP
Artigos e Materiais de Revistas Científicas - LIM/24
Artigos e Materiais de Revistas Científicas - LIM/31
Artigos e Materiais de Revistas Científicas - ODS/03