Abstract

Abstract Accumulating evidence suggests that DNA repair enzyme activity may predict sensitivity to chemotherapeutic agents in cancer cells. The status of a DNA repair enzyme, such as XPF/ERCC4 or XPD/ERCC2, has been reported to serve as a prognostic indicator as well as an indicator of chemosensitivity. Another such candidate is the protein product of the DDB2 gene, p48, that interacts with the p127 protein to form the UV-damaged DNA binding complex (DDB). DDB2, a DNA repair factor induced by tumor suppressor p53, plays an important role in the nucleotide excision repair (NER) of UV-damaged DNA. Mice lacking DDB2 developed spontaneous tumors at a high rate, suggesting a tumor suppression function for DDB2. In this study, we hypothesized that DDB2 expression correlated with sensitivity to chemotherapeutic agents. To this end, we compared the cytotoxicity levels of DDB2-expressing and non-expressing cell lines upon exposure to chemotherapeutic agents. As a result, downregulation of DDB2 using siRNA restored chemosensitivity. DDB2 may be a molecular marker for prediction of chemosensitivity and a new target molecule for cancer chemotherapy. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3936.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.