The Mechanisms Underlying the Increased Radiosensitivity of HPV-Related Tumor Cells

The important role of virus on carcinogenesis is well understood. The exist of virus within tumor cells could affect the tumor response to anti-cancer therapy. For example, in head and neck squamous cell carcinoma, especially in the oropharyngeal cancer, patients with human papilloma virus (HPV) infections have about 30% better overall survival rates than those without infections after chemotherapy and radiotherapy. This conclusion has been demonstrated by several similar studies. However, the underlying mechanisms that HPV infections increase radiosensitivity are still unclear. HPV could be found in most patients with cervical cancer. Few cervical cancer patients without HPV infections also had poor prognosis. The results of our recent clinical studies showed that patients with different genotypes of HPV had different treatment response to radiotherapy or chemoradiotherapy. These clinical observations are worth to further exploring. In this projection, cervical cancer cell lines with different HPV will be used to analyze the cellular response to radiation damage. We hypothesize that the changes of DNA repair mechanisms after virus infection result in increasing cellular radiosensitivity. Therefore, we will examine the capability of DNA repair on different cervical cancer cell lines and determine the effect of viral proteins on this mechanism. Another hypothesis is that radiation-induced viral gene expression injuries tumor cells. To examine this hypothesis, we will quantity the change of viral gene expression after irradiation in cell lines. Furthermore, some clinical samples with the patients’ consent will be analyzed for this hypothesis. The results of this study will help us to understand the cell response after radiation exposure. In clinic practice, it could enhance our ability to predict the treatment outcome in various cancer.

Project ID:PC10207-0826
External Project ID:NSC102-2314-B182-061