@article{42888b572a4349a38e74bc8bbd728313,
title = "Inactivation of XPF Sensitizes Cancer Cells to Gemcitabine",
abstract = "Gemcitabine (2′, 2′-difluorodeoxycytidine; dFdC) is a deoxycytidine analog and is used primarily against pancreatic cancer. The cytotoxicity of gemcitabine is due to the inhibition of DNA replication. However, a mechanism of removal of the incorporated dFdC is largely unknown. In this report, we discovered that nucleotide excision repair protein XPF-ERCC1 participates in the repair of gemcitabine-induced DNA damage and inactivation of XPF sensitizes cells to gemcitabine. Further analysis identified that XPF-ERCC1 functions together with apurinic/apyrimidinic endonuclease (APE) in the repair of gemcitabine-induced DNA damage. Our results demonstrate the importance of the evaluation of DNA repair activities in gemcitabine treatment.",
author = "George, {Joseph W.} and Mika Bessho and Tadayoshi Bessho",
note = "Funding Information: We thank Dr. Toshiyasu Taniguchi (Tokai University, Japan) for ovarian cancer cell lines PE01 and PE01(C4-2) and pancreatic cancer cell lines CAPAN1 and CAPAN1(C2-1) and Dr. Kishor K. Bhakat (Department of Genetics, Cell Biology and Anatomy at University of Nebraska Medical Center) for colon cancer cell lines HCT116 and HCT116 shAPE. We also thank two Eppley Institute Summer Undergraduate Research Program students, Jacquelyn Peck (Creighton University, Omaha, NE) and Anthony Cloyd (Hasting Collage, Hasting, NE) for their technical contributions in some experiments. This work was supported in part by the Fred & Pamela Buffett Cancer Center Support Grant from the National Cancer Institute under award no. P30 CA036727. Publisher Copyright: {\textcopyright} 2019 Joseph W. George et al.",
year = "2019",
doi = "10.1155/2019/6357609",
language = "English (US)",
volume = "2019",
journal = "Journal of Nucleic Acids",
issn = "2090-0201",
publisher = "Hindawi Publishing Corporation",
}