Tobacco smoke activates human papillomavirus 16 p97 promoter and cooperates with high-risk E6/E7 for oxidative DNA damage in lung cells.

Nelson Peña; Diego Carrillo; Juan P. Muñoz; Jonás Chnaiderman; Ulises Urzúa; Oscar León; Tornesello Maria L.; Corvalán Alejandro H.; Ricardo Soto-Rifo; Francisco Aguayo

doi:10.1371/journal.pone.0123029

Tobacco smoke activates human papillomavirus 16 p97 promoter and cooperates with high-risk E6/E7 for oxidative DNA damage in lung cells.

Título traducido de la contribución: El humo del tabaco activa el promotor p97 del virus del papiloma humano 16 y coopera con el E6/E7 de alto riesgo para el daño oxidativo del ADN en las células pulmonares.

Nelson Peña
, Diego Carrillo
, Juan P. Muñoz
, Jonás Chnaiderman
, Ulises Urzúa
, Oscar León
, Tornesello Maria L.
, Corvalán Alejandro H.
, Ricardo Soto-Rifo
, Francisco Aguayo

Producción científica: Contribución a una revista › Artículo › revisión exhaustiva

31 Citas (Scopus)

Resumen

Hemos demostrado previamente una interacción funcional entre las oncoproteínas E6 y E7 del virus del papiloma humano tipo 16 (HPV-16) y el condensado de humo de cigarrillo (CSC) en células pulmonares, lo que sugiere cooperación durante la carcinogénesis. Sin embargo, los mecanismos moleculares de dicha interacción aún no se han dilucidado. Aquí presentamos primero evidencia que muestra que el condensado de humo de cigarrillo (CSC) tiene la capacidad de activar el promotor p97 de HPV-16 al actuar sobre la región de control larga (LCR) en las células epiteliales pulmonares. Curiosamente, observamos que la activación del promotor p97 inducida por CSC ocurre de manera dependiente de la dosis en células tumorales A-549 (adenocarcinoma de pulmón), H-2170 (carcinoma bronquial), SiHa o Hela (carcinoma cervical), pero no en células pulmonares no tumorales BEAS-2B (bronquiales) o NL-20 (alveolares), a menos que expresen ectópicamente los oncogenes E6 y E7 de HPV-16. Además, observamos un aumento significativo del daño primario al ADN en células pulmonares tumorales y no tumorales tratadas con CSC que expresan los oncogenes E6 y E7 del VPH-16, lo que sugiere un efecto cooperativo en este proceso, a pesar de que la contribución del E7 fue significativamente mayor. En conjunto, nuestros resultados sugieren firmemente que el humo del tabaco puede inducir la activación del promotor p97 del VPH-16 en cooperación con los oncogenes E6 y E7 del VPH-16, que, a su vez, sensibilizan a las células pulmonares al daño al ADN inducido por el humo del tabaco.

Título traducido de la contribución	El humo del tabaco activa el promotor p97 del virus del papiloma humano 16 y coopera con el E6/E7 de alto riesgo para el daño oxidativo del ADN en las células pulmonares.
Idioma original	Inglés
Número de artículo	e0123029
Publicación	PLoS ONE
Volumen	10
N.º	4
DOI	https://doi.org/10.1371/journal.pone.0123029
Estado	Publicada - 1 abr. 2015
Publicado de forma externa	Sí

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@article{926dd5862757469e844343bc20d124b0,

title = "Tobacco smoke activates human papillomavirus 16 p97 promoter and cooperates with high-risk E6/E7 for oxidative DNA damage in lung cells.",

abstract = "We have previously shown a functional interaction between human papillomavirus type 16 (HPV-16) E6 and E7 oncoproteins and cigarette smoke condensate (CSC) in lung cells suggesting cooperation during carcinogenesis. The molecular mechanisms of such interaction, however, remain to be elucidated. Here we first present evidence showing that cigarette smoke condensate (CSC) has the ability to activate the HPV-16 p97 promoter by acting on the long control region (LCR) in lung epithelial cells. Interestingly, we observed that CSC-induced p97 promoter activation occurs in a dose-dependent manner in both tumor A-549 (lung adenocarcinoma), H-2170 (bronchial carcinoma), SiHa or Hela (cervical carcinoma) cells but not in non-tumor BEAS-2B (bronchial) or NL-20 (alveolar) lung cells unless they ectopically expressed the HPV-16 E6 and E7 oncogenes. In addition, we also observed a significant increase of primary DNA damage in tumor and non-tumor CSC-treated lung cells expressing HPV-16 E6 and E7 oncogenes suggesting a cooperative effect in this process, even though the contribution of E7 was significantly higher. Taken together, our results strongly suggest that tobacco smoke is able to induce the activation of the HPV-16 p97 promoter in cooperation with HPV-16 E6 and E7 oncogenes that, in turn, sensitize lung cells to tobacco smoke-induced DNA damage.",

author = "Nelson Pe{\~n}a and Diego Carrillo and Mu{\~n}oz, \{Juan P.\} and Jon{\'a}s Chnaiderman and Ulises Urz{\'u}a and Oscar Le{\'o}n and \{Maria L.\}, Tornesello and \{Alejandro H.\}, Corval{\'a}n and Ricardo Soto-Rifo and Francisco Aguayo",

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T1 - Tobacco smoke activates human papillomavirus 16 p97 promoter and cooperates with high-risk E6/E7 for oxidative DNA damage in lung cells.

AU - Peña, Nelson

AU - Carrillo, Diego

AU - Muñoz, Juan P.

AU - Chnaiderman, Jonás

AU - Urzúa, Ulises

AU - León, Oscar

AU - Maria L., Tornesello

AU - Alejandro H., Corvalán

AU - Soto-Rifo, Ricardo

AU - Aguayo, Francisco

PY - 2015/4/1

Y1 - 2015/4/1

N2 - We have previously shown a functional interaction between human papillomavirus type 16 (HPV-16) E6 and E7 oncoproteins and cigarette smoke condensate (CSC) in lung cells suggesting cooperation during carcinogenesis. The molecular mechanisms of such interaction, however, remain to be elucidated. Here we first present evidence showing that cigarette smoke condensate (CSC) has the ability to activate the HPV-16 p97 promoter by acting on the long control region (LCR) in lung epithelial cells. Interestingly, we observed that CSC-induced p97 promoter activation occurs in a dose-dependent manner in both tumor A-549 (lung adenocarcinoma), H-2170 (bronchial carcinoma), SiHa or Hela (cervical carcinoma) cells but not in non-tumor BEAS-2B (bronchial) or NL-20 (alveolar) lung cells unless they ectopically expressed the HPV-16 E6 and E7 oncogenes. In addition, we also observed a significant increase of primary DNA damage in tumor and non-tumor CSC-treated lung cells expressing HPV-16 E6 and E7 oncogenes suggesting a cooperative effect in this process, even though the contribution of E7 was significantly higher. Taken together, our results strongly suggest that tobacco smoke is able to induce the activation of the HPV-16 p97 promoter in cooperation with HPV-16 E6 and E7 oncogenes that, in turn, sensitize lung cells to tobacco smoke-induced DNA damage.

AB - We have previously shown a functional interaction between human papillomavirus type 16 (HPV-16) E6 and E7 oncoproteins and cigarette smoke condensate (CSC) in lung cells suggesting cooperation during carcinogenesis. The molecular mechanisms of such interaction, however, remain to be elucidated. Here we first present evidence showing that cigarette smoke condensate (CSC) has the ability to activate the HPV-16 p97 promoter by acting on the long control region (LCR) in lung epithelial cells. Interestingly, we observed that CSC-induced p97 promoter activation occurs in a dose-dependent manner in both tumor A-549 (lung adenocarcinoma), H-2170 (bronchial carcinoma), SiHa or Hela (cervical carcinoma) cells but not in non-tumor BEAS-2B (bronchial) or NL-20 (alveolar) lung cells unless they ectopically expressed the HPV-16 E6 and E7 oncogenes. In addition, we also observed a significant increase of primary DNA damage in tumor and non-tumor CSC-treated lung cells expressing HPV-16 E6 and E7 oncogenes suggesting a cooperative effect in this process, even though the contribution of E7 was significantly higher. Taken together, our results strongly suggest that tobacco smoke is able to induce the activation of the HPV-16 p97 promoter in cooperation with HPV-16 E6 and E7 oncogenes that, in turn, sensitize lung cells to tobacco smoke-induced DNA damage.

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Tobacco smoke activates human papillomavirus 16 p97 promoter and cooperates with high-risk E6/E7 for oxidative DNA damage in lung cells.

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