Abstract
Background:We have previously shown that stable transfection of the human papillomavirus (HPV) E6*I oncogene can sensitize two HPV negative oropharyngeal cancer (OSCC) cell lines to radiation. In the current study, we extended our work on OSCC to determine whether the HPV E6 oncogene can enhance the radiosensitivity of non-OSCC cell lines.Methods:Three non-OSCC cell lines (melanoma, colorectal adenocarcinoma and large cell lung cancer) were stably transfection with the HPV E6 oncogene (E6 total, E6*I and E6*II) and treated with different doses of radiation. Clonogenic assays were used to measure the radiation survival.Results:Following transfection, there was a reduction in the survival of the melanoma cell line after 2 Gy (SF2) from 0.401 (untransfected) to 0.219 (Melanoma-E6 total). This reduction was not evident at higher doses of radiation. There was no significant change in the SF2 of melanoma-E6*I (0.303) and melanoma-E6*II (0.414). The SF2 colorectal adenocarcinoma and large cell lung cancer cell lines did not change significantly after transfection.Conclusions: The radiosensitizing effect of HPV E6 oncogene is cell line specific. We found no clear evidence of a radiosensitising effect of E6 in these three non-OSCC cancer cell lines.
Highlights
Viral infectious diseases and cancer are both pandemics and it has been estimated that over 15% of all cancers worldwide are related to infection by virus; e.g. oropharyngeal squamous cell carcinoma (OSCC) and cervix with human papillomavirus (HPV), nasopharyngeal carcinoma with Epstein-Barr virus, and Kaposi’s sarcoma with human herpes virus 8
We found no clear evidence of a radiosensitising effect of E6 in these three non-OSCC cancer cell lines
We extended our work on OSCC to determine whether the HPV E6 oncogene can enhance the radiosensitivity of non-OSCC cell lines
Summary
Viral infectious diseases and cancer are both pandemics and it has been estimated that over 15% of all cancers worldwide are related to infection by virus; e.g. oropharyngeal squamous cell carcinoma (OSCC) and cervix with human papillomavirus (HPV), nasopharyngeal carcinoma with Epstein-Barr virus, and Kaposi’s sarcoma with human herpes virus 8. Radiation therapy plays an important role in the management of these viral-related malignancies and they are all relatively radiosensitive clinically. The impact of viral infection on the response of cancer to radiotherapy is critical in the field of radiation biology. We have previously shown that stable transfection of the human papillomavirus (HPV) E6*I oncogene can sensitize two HPV negative oropharyngeal cancer (OSCC) cell lines to radiation. We extended our work on OSCC to determine whether the HPV E6 oncogene can enhance the radiosensitivity of non-OSCC cell lines
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