FGFR3-induced Y158 PARP1 phosphorylation promotes PARP inhibitor resistance via BRG1/MRE11-mediated DNA repair in breast cancer models - Chen, Mei-Kuang; Yamaguchi, Hirohito; Gao, Yuan; Xia, Weiya; Chang, Jeffrey T.; Hsiao, Yu-Chun; Shegute, Tewodros W.; Lin, Zong-Shin; Wu, Chen-Shiou; Wang, Yu-Han; Litton, Jennifer K.; Ding, Qingqing; et al. (The Journal of clinical investigation, 2025)
Keywords: Animals; Cell Line, Tumor; DNA Helicases - genetics; DNA Helicases - metabolism; DNA Repair - drug effects; Drug Resistance, Neoplasm; Female; Humans; Mice; MRE11 Homologue Protein - genetics; MRE11 Homologue Protein - metabolism; Neoplasm Proteins - genetics; Neoplasm Proteins - metabolism; Nuclear Proteins - genetics; Nuclear Proteins - metabolism; Phosphorylation - drug effects; Poly (ADP-Ribose) Polymerase-1 - genetics; Poly (ADP-Ribose) Polymerase-1 - metabolism; Poly(ADP-ribose) Polymerase Inhibitors - pharmacology; Receptor, Fibroblast Growth Factor, Type 3 - genetics; Receptor, Fibroblast Growth Factor, Type 3 - metabolism; Transcription Factors - genetics; Transcription Factors - metabolism; Triple Negative Breast Neoplasms - drug therapy; Triple Negative Breast Neoplasms - genetics; Triple Negative Breast Neoplasms - metabolism; Triple Negative Breast Neoplasms - pathology; Xenograft Model Antitumor Assays; Oncology; Breast cancer; Drug therapy; Protein kinases; Therapeutics