HPV-Mediated Resistance to TNF and TRAIL Is Characterized by Global Alterations in Apoptosis Regulatory Factors, Dysregulation of Death Receptors, and Induction of ROS/RNS

Imagem de Miniatura
Arquivos
art_CABECA_HPVMediated_Resistance_to_TNF_and_TRAIL_Is_Characterized_2019.PDF (3.43 MB)
Citações na Scopus
17
Tipo de produção
article
Data de publicação
2019
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
MDPI
Autores
CABECA, Tatiane Karen
ABREU, Alice de Mello
ANDRETTE, Rafael
LINO, Vanesca de Souza
AGUAYO, Francisco
LEPIQUE, Ana Paula
BOCCARDO, Enrique
Citação
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.20, n.1, article ID 198, 17p, 2019
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Persistent infection with high-risk human papilloma virus (HR-HPV) is the main risk factor for the development of invasive cervical cancer although is not sufficient to cause cervical cancer. Several host and environmental factors play a key role in cancer initiation/progression, including cytokines and other immune-response mediators. Here, we characterized the response to the individual and combined action of the pro-inflammatory cytokines tumor necrosis factor (TNF) and TNF-related apoptosis-inducing ligand (TRAIL) on HPV-transformed cells and human keratinocytes ectopically expressing E6 and E7 early proteins from different HPV types. We showed that keratinocytes expressing HPV early proteins exhibited global alterations in the expression of proteins involved in apoptosis regulation/execution, including TNF and TRAIL receptors. Besides, we provided evidence that TNF receptor 1 (TNFR1) was down-regulated and may be retained in the cytoplasm of keratinocytes expressing HPV16 oncoproteins. Finally, fluorescence analysis demonstrated that cytokine treatment induced the production and release of reactive oxygen and nitrogen species (ROS/RNS) in cells expressing HPV oncogenes. Alterations in ROS/RNS production and apoptosis regulatory factors expression in response to inflammatory mediators may favor the accumulation of genetic alterations in HPV-infected cells. Altogether, our results suggested that these events may contribute to lesion progression and cancer onset.
Palavras-chave
HPV, TNF, TRAIL, apoptosis, ROS, RNS
URI
https://observatorio.fm.usp.br/handle/OPI/31144
Referências
  1. Banerjee NS, 2006, J VIROL, V80, P6517, DOI 10.1128/JVI.02499-05
  2. Basile JR, 2001, J BIOL CHEM, V276, P22522, DOI 10.1074/jbc.M010505200
  3. Benedict CA, 2003, CYTOKINE GROWTH F R, V14, P349, DOI 10.1016/S1359-6101(03)00030-3
  4. Benedict CA, 2002, NAT IMMUNOL, V3, P1013, DOI 10.1038/ni1102-1013
  5. Bhat P, 2011, IMMUNOL REV, V239, P85, DOI 10.1111/j.1600-065X.2010.00966.x
  6. Bhattacharya S, 1999, GENE DEV, V13, P64, DOI 10.1101/gad.13.1.64
  7. Boccardo E, 2004, VIROLOGY, V328, P233, DOI 10.1016/j.virol.2004.07.026
  8. Boccardo E, 2010, CARCINOGENESIS, V31, P521, DOI 10.1093/carcin/bgp333
  9. Bodily JM, 2011, CANCER RES, V71, P1187, DOI 10.1158/0008-5472.CAN-10-2626
  10. Borbely AA, 2006, J GEN VIROL, V87, P287, DOI 10.1099/vir.0.81067-0
  11. Chamulitrat W, 2009, EXP DERMATOL, V18, P1067, DOI 10.1111/j.1600-0625.2009.00888.x
  12. Chaturvedi V, 1999, J BIOL CHEM, V274, P23358, DOI 10.1074/jbc.274.33.23358
  13. De Marco F, 2013, VIRUSES-BASEL, V5, P708, DOI 10.3390/v5020708
  14. Doorbar J, 2018, BEST PRACT RES CL OB, V47, P27, DOI 10.1016/j.bpobgyn.2017.08.001
  15. Duerksen-Hughes PJ, 1999, VIROLOGY, V264, P55, DOI 10.1006/viro.1999.9977
  16. ETTEHADI P, 1994, CLIN EXP IMMUNOL, V96, P146, DOI 10.1111/j.1365-2249.1994.tb06244.x
  17. Freedman SJ, 2003, NAT STRUCT BIOL, V10, P504, DOI 10.1038/nsb936
  18. Garnett TO, 2006, CELL DEATH DIFFER, V13, P1915, DOI 10.1038/sj.cdd.4401886
  19. Ghosh S, 2002, CELL, V109, pS81, DOI 10.1016/S0092-8674(02)00703-1
  20. Goodwin EC, 1998, J VIROL, V72, P3925
  21. Guess JC, 2005, J VIROL, V79, P14852, DOI 10.1128/JVI.79.23.14852-14862.2005
  22. HAGARI Y, 1995, J INVEST DERMATOL, V104, P526, DOI 10.1111/1523-1747.ep12606028
  23. HAWLEYNELSON P, 1989, EMBO J, V8, P3905, DOI 10.1002/j.1460-2075.1989.tb08570.x
  24. Helt AM, 2001, J VIROL, V75, P6737, DOI 10.1128/JVI.75.15.6737-6747.2001
  25. Hu YL, 2001, NATURE, V410, P710, DOI 10.1038/35070605
  26. James MA, 2006, J VIROL, V80, P5301, DOI 10.1128/JVI.01942-05
  27. Jian YC, 1998, ONCOGENE, V17, P2027, DOI 10.1038/sj.onc.1202142
  28. Jin ZY, 2006, MOL CELL BIOL, V26, P8136, DOI 10.1128/MCB.00257-06
  29. Jung YJ, 2003, FASEB J, V17, P2115, DOI 10.1096/fj.03-0329fje
  30. Kabsch K, 2004, INTERVIROLOGY, V47, P48, DOI 10.1159/000076642
  31. Kaltschmidt B, 1999, ONCOGENE, V18, P3213, DOI 10.1038/sj.onc.1202657
  32. Komine M, 2000, J BIOL CHEM, V275, P32077, DOI 10.1074/jbc.M001253200
  33. Kondo S, 1997, EUR J IMMUNOL, V27, P1713, DOI 10.1002/eji.1830270718
  34. Mittal S, 2017, MUTAT RES-REV MUTAT, V772, P23, DOI 10.1016/j.mrrev.2016.08.001
  35. Moody CA, 2007, P NATL ACAD SCI USA, V104, P19541, DOI 10.1073/pnas.0707947104
  36. MUNGER K, 1989, J VIROL, V63, P4417
  37. Nakamura M, 2009, VIROLOGY, V387, P442, DOI 10.1016/j.virol.2009.02.036
  38. Natoli G, 1998, J BIOL CHEM, V273, P31262, DOI 10.1074/jbc.273.47.31262
  39. Nees M, 2001, J VIROL, V75, P4283, DOI 10.1128/JVI.75.9.4283-4296.2001
  40. Prabhavathy D, 2015, BIOSCIENCE REP, V35, DOI 10.1042/BSR20140160
  41. Reiser J, 2011, J VIROL, V85, P11372, DOI 10.1128/JVI.05279-11
  42. Rodolico V, 2011, INFECT AGENTS CANCER, V6, DOI 10.1186/1750-9378-6-18
  43. Schiffman M, 2016, NAT REV DIS PRIMERS, V2, DOI 10.1038/nrdp.2016.86
  44. Schlecht NF, 2001, JAMA-J AM MED ASSOC, V286, P3106, DOI 10.1001/jama.286.24.3106
  45. Seitz CS, 2000, CANCER RES, V60, P4085
  46. Seitz CS, 1998, P NATL ACAD SCI USA, V95, P2307, DOI 10.1073/pnas.95.5.2307
  47. Spitkovsky D, 2002, J BIOL CHEM, V277, P25576, DOI 10.1074/jbc.M201884200
  48. Termini L, 2018, CURR TOP MED CHEM, V18, P246, DOI 10.2174/1568026618666180410125850
  49. Ting AT, 2016, TRENDS IMMUNOL, V37, P535, DOI 10.1016/j.it.2016.06.002
  50. van Hogerlinden M, 1999, CANCER RES, V59, P3299
  51. Vanamee ES, 2018, SCI SIGNAL, V11, DOI 10.1126/scisignal.aao4910
  52. Vieira KBL, 1996, CANCER RES, V56, P2452
  53. VILLA LL, 1992, MOL CARCINOGEN, V6, P5, DOI 10.1002/mc.2940060103
  54. Wang SL, 2003, ONCOGENE, V22, P8628, DOI 10.1038/sj.onc.1207232
  55. ZerfassThome K, 1996, ONCOGENE, V13, P2323

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