ArticleFrontiers in microbiology2018
Tobacco Exposure Enhances Human Papillomavirus 16 Oncogene Expression via EGFR/PI3K/Akt/c-Jun Signaling Pathway in Cervical Cancer Cells.
Article in Frontiers in microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 46 citations in OpenAlex.
- From Motor Proteins to Oncogenic Factors: The Evolving Role of Kinesin Superfamily Proteins in Breast Cancer Development.Molecular biotechnology · 2026Review
- Dynamics of Cervical Lesions After Excisional Treatment in Relation to HPV Genotypes and Cytological Findings.Journal of clinical medicine · 2026Article
- Elevated Prevalence of Oral HPV Infection Among Females with Periodontitis: A Cross-Sectional Study.Oral health & preventive dentistry · 2026Article
- Human Papillomavirus and Other Relevant Issues in Cervical Cancer Pathogenesis.International journal of molecular sciences · 2025Review
- HPV and Cervical Cancer-Biology, Prevention, and Treatment Updates.Current oncology (Toronto, Ont.) · 2025Review
- Impact of Smoking on Cervical Histopathological Changes in High-Risk HPV-Positive Women: A Matched Case-Control Study.Medicina (Kaunas, Lithuania) · 2025Article
- Downregulated CCND3 Is a Key Event Driving Lung Adenocarcinoma Metastasis during Acquired Cisplatin Resistance.International journal of biological sciences · 2025Article
- Causal Effects of Smoking, Alcohol, Coffee, and Tea Intake on Gynecologic Cancers: A Mendelian Randomization Study.International journal of women's health · 2025Article
- SLC7A11 Expression Is Up-Regulated in HPV- and Tobacco-Associated Lung Cancer.International journal of molecular sciences · 2024Article
- Curcumin attenuates smoking and drinking activated NF-κB/IL-6 inflammatory signaling axis in cervical cancer.Cancer cell international · 2024Article
- Epstein-Barr Virus BARF1 Is Expressed in Lung Cancer and Is Associated with Cancer Progression.Cells · 2024Article
- KIFC3 promotes the proliferation, migration and invasion of non-small cell lung cancer through the PI3K/AKT signaling pathway.Scientific reports · 2024Article
- Human Papilloma Virus Positive Oropharyngeal Squamous Cell Carcinoma and the Immune System: Pathogenesis, Immunotherapy and Future Perspectives.International journal of molecular sciences · 2024Review
- ErbB2/HER2 receptor tyrosine kinase regulates human papillomavirus promoter activity.Frontiers in immunology · 2024Article
- Human papillomavirus associated cervical lesion: pathogenesis and therapeutic interventions.MedComm · 2023Review
- 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
- Human papillomavirus in the setting of immunodeficiency: Pathogenesis and the emergence of next-generation therapies to reduce the high associated cancer risk.Frontiers in immunology · 2023Review
- Characterization of High-Risk HPV/EBV Co-Presence in Pre-Malignant Cervical Lesions and Squamous Cell Carcinomas.Microorganisms · 2022Article
- Article
- Dysregulation of the miR-30a/BiP axis by cigarette smoking accelerates oral cancer progression.Cancer cell international · 2021Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-risk human papillomavirus (HR-HPV) infection is not a sufficient condition for cervical cancer development because most infections are benign and naturally cleared. Epidemiological studies revealed that tobacco smoking is a cofactor with HR-HPV for cervical cancer initiation and progression, even though the mechanism by which tobacco smoke cooperates with HR-HPV in this malignancy is poorly understood. As HR-HPV E6/E7 oncoproteins overexpressed in cervical carcinomas colocalize with cigarette smoke components (CSC), in this study we addressed the signaling pathways involved in a potential interaction between both carcinogenic agents. Cervical cancer-derived cell lines, CaSki (HPV16; 500 copies per cell) and SiHa (HPV16; 2 copies per cell), were acutely exposed to CSC at various non-toxic concentrations and we found that E6 and E7 levels were significantly increased in a dose-dependent manner. Using a reporter construct containing the luciferase gene under the control of the full HPV16 long control region (LCR), we also found that p97 promoter activity is dependent on CSC. Non-synonymous mutations in the LCR-resident TPA (12-O-tetradecanoylphorbol 13-acetate)-response elements (TRE) had significantly decreased p97 promoter activation. Phosphoproteomic arrays and specific inhibitors revealed that CSC-mediated E6/E7 overexpression is at least in part reliant on EGFR phosphorylation. In addition, we showed that the PI3K/Akt pathway is crucial for CSC-induced E6/E7 overexpression. Finally, we demonstrated that HPV16 E6/E7 overexpression is mediated by JUN. overexpression, c-Jun phosphorylation and recruitment of this transcription factor to TRE sites in the HPV16 LCR. We conclude that acute exposure to tobacco smoke activates the transcription of HPV16 E6 and E7 oncogenes through p97 promoter activation, which involves the EGFR/PI3K/Akt/C-Jun signaling pathway activation in cervical cancer cells.
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