Functional Interaction between Human Papillomavirus Type 16 E6 and E7 Oncoproteins and Cigarette Smoke Components in Lung Epithelial Cells

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dc.contributor.authorPablo Munoz, Juan
dc.contributor.authorGonzalez, Carolina
dc.contributor.authorParra, Barbara
dc.contributor.authorCorvalan, Alejandro H.
dc.contributor.authorTornesello, Maria Lina
dc.contributor.authorEizuru, Yoshito
dc.contributor.authorAguayo, Francisco
dc.date.accessioned2024-01-10T12:39:08Z
dc.date.available2024-01-10T12:39:08Z
dc.date.issued2012
dc.description.abstractThe smoking habit is the most important, but not a sufficient cause for lung cancer development. Several studies have reported the human papillomavirus type 16 (HPV16) presence and E6 and E7 transcripts expression in lung carcinoma cases from different geographical regions. The possible interaction between HPV infection and smoke carcinogens, however, remains unclear. In this study we address a potential cooperation between tobacco smoke and HPV16 E6 and E7 oncoproteins for alterations in proliferative and tumorigenic properties of lung epithelial cells. A549 (alveolar, tumoral) and BEAS-2B (bronchial, non-tumoral) cell lines were stably transfected with recombinant pLXSN vectors expressing HPV16 E6 and E7 oncoproteins and exposed to cigarette smoke condensate (CSC) at different concentrations. HPV16 E6 and E7 expression was associated with loss of p53 stability, telomerase (hTERT) and p16(INK4A) overexpression in BEAS-2B cells as demonstrated by quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting (WB). In A549 cells we observed downregulation of p53 but not a significant increase of hTERT transcripts. In addition, the HPV16 E6/E7 transfected cell lines showed an increased proliferation rate and anchorage-independent growth in a HPV16 E6 and E7 expression-dependent manner. Moreover, both HPV16 E6/E7 and mock transfected cells showed an increased proliferation rate and anchorage-independent growth in the presence of 0.1 and 10 mu g/mL CSC. However, this increase was significantly greater in HPV16 E6/E7 transfected cells (p<0.001). Data were confirmed by FCSE proliferation assay. The results obtained in this study are suggestive of a functional interaction between tobacco smoke and HPV16 E6/E7 oncoproteins for malignant transformation and tumorigenesis of lung epithelial cells. More studies are warranted in order to dissect the molecular mechanisms involved in this cooperation.
dc.description.funderFondecyt from the government of Chile
dc.fechaingreso.objetodigital2024-05-07
dc.format.extent10 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1371/journal.pone.0038178
dc.identifier.issn1932-6203
dc.identifier.pubmedidMEDLINE:22662279
dc.identifier.urihttps://doi.org/10.1371/journal.pone.0038178
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/77150
dc.identifier.wosidWOS:000305342300171
dc.information.autorucMedicina;Corvalan A;S/I;63885
dc.issue.numero5
dc.language.isoen
dc.nota.accesoSin adjunto
dc.publisherPUBLIC LIBRARY SCIENCE
dc.revistaPLOS ONE
dc.rightsregistro bibliográfico
dc.subjectCERVICAL-CANCER
dc.subjectORAL CARCINOGENESIS
dc.subjectCARCINOMAS
dc.subjectINFECTION
dc.subjectHPV
dc.subjectMECHANISMS
dc.subjectNICOTINE
dc.subjectPROLIFERATION
dc.subjectINVOLVEMENT
dc.subjectPROTEINS
dc.subject.ods03 Good Health and Well-being
dc.subject.ods05 Gender Equality
dc.subject.odspa03 Salud y bienestar
dc.subject.odspa05 Igualdad de género
dc.titleFunctional Interaction between Human Papillomavirus Type 16 E6 and E7 Oncoproteins and Cigarette Smoke Components in Lung Epithelial Cells
dc.typeartículo
dc.volumen7
sipa.codpersvinculados63885
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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