ArticlePloS one2015
Tobacco smoke activates human papillomavirus 16 p97 promoter and cooperates with high-risk E6/E7 for oxidative DNA damage in lung cells.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Evidence for Anal Dysplasia Treatment.Clinics in colon and rectal surgery · 2026Review
- An open-source multi-semantic annotation dataset and automated recognition tool for viral carcinogenesis factors.Database : the journal of biological databases and curation · 2025Article
- SLC7A11 Expression Is Up-Regulated in HPV- and Tobacco-Associated Lung Cancer.International journal of molecular sciences · 2024Article
- Epstein-Barr Virus BARF1 Is Expressed in Lung Cancer and Is Associated with Cancer Progression.Cells · 2024Article
- Article
- The Role of Human Papilloma Virus (HPV) in Primary Lung Cancer Development: State of the Art and Future Perspectives.Life (Basel, Switzerland) · 2024Review
- Interaction between Cigarette Smoke and Human Papillomavirus 16 E6/E7 Oncoproteins to Induce SOD2 Expression and DNA Damage in Head and Neck Cancer.International journal of molecular sciences · 2023Article
- Review
- Cellular and Molecular Signatures of Oxidative Stress in Bronchial Epithelial Cell Models Injured by Cigarette Smoke Extract.International journal of molecular sciences · 2022Review
- Interplay between Epstein-Barr virus infection and environmental xenobiotic exposure in cancer.Infectious agents and cancer · 2021Review
- Chemopreventive Role of Apigenin against the Synergistic Carcinogenesis of Human Papillomavirus and 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone.Biomedicines · 2020Article
- Risk of HPV-related extra-cervical cancers in women treated for cervical intraepithelial neoplasia.BMC cancer · 2020Article
- Role of Epstein-Barr Virus and Human Papillomavirus Coinfection in Cervical Cancer: Epidemiology, Mechanisms and Perspectives.Pathogens (Basel, Switzerland) · 2020Review
- High-Risk Human Papillomavirus and Tobacco Smoke Interactions in Epithelial Carcinogenesis.Cancers · 2020Review
- Possible Oncogenic Viruses Associated with Lung Cancer.OncoTargets and therapy · 2020Review
- CYP1A1 methylation mediates the effect of smoking and occupational polycyclic aromatic hydrocarbons co-exposure on oxidative DNA damage among Chinese coke-oven workers.Environmental health : a global access science source · 2019Article
- Regulation of HPV transcription.Clinics (Sao Paulo, Brazil) · 2018Review
- Tobacco Exposure Enhances Human Papillomavirus 16 Oncogene Expression via EGFR/PI3K/Akt/c-Jun Signaling Pathway in Cervical Cancer Cells.Frontiers in microbiology · 2018Article
- Upregulation of PIR gene expression induced by human papillomavirus E6 and E7 in epithelial oral and cervical cells.Open biology · 2017Article
- Smoking modify the effects of polycyclic aromatic hydrocarbons exposure on oxidative damage to DNA in coke oven workers.International archives of occupational and environmental health · 2017Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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