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
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Citações na Scopus
19
Tipo de produção
article
Data de publicação
2019
Editora
MDPI
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Título do Volume
Autores
CABECA, Tatiane Karen
ABREU, Alice de Mello
ANDRETTE, Rafael
LINO, Vanesca de Souza
AGUAYO, Francisco
LEPIQUE, Ana Paula
BOCCARDO, Enrique
Autor de Grupo de pesquisa
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Organizadores
Citação
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.20, n.1, article ID 198, 17p, 2019
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
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