PT - JOURNAL ARTICLE AU - KUAN-HAO CHEN AU - ZIH-YIN LAI AU - DING-YU LI AU - YU-CHUAN LIN AU - FONG-IN CHOU AU - YUNG-JEN CHUANG TI - Analysis of DNA Damage Responses After Boric Acid-mediated Boron Neutron Capture Therapy in Hepatocellular Carcinoma AID - 10.21873/anticanres.13881 DP - 2019 Dec 01 TA - Anticancer Research PG - 6661--6671 VI - 39 IP - 12 4099 - http://ar.iiarjournals.org/content/39/12/6661.short 4100 - http://ar.iiarjournals.org/content/39/12/6661.full SO - Anticancer Res2019 Dec 01; 39 AB - Background: Boron neutron capture therapy (BNCT) selectively kills tumor cells while sparing adjacent normal cells. Boric acid (BA)-mediated BNCT showed therapeutic efficacy in treating hepatocellular carcinoma (HCC) in vivo. However, DNA damage and corresponding responses induced by BA-mediated BNCT remained unclear. This study aimed to investigate whether BA-mediated BNCT induced DNA double-strand breaks (DSBs) and to explore DNA damage responses in vitro. Materials and Methods: Huh7 Human HCC cells were treated with BA and irradiated with neutrons during BA-BNCT. Cell survival and DNA DSBs were examined by clonogenic assay and expression of phosphorylated H2A histone family member X (γH2AX), respectively. The DNA damage response was explored by determining the expression levels of DNA repair- and apoptosis-associated proteins and conducting a cell-cycle analysis. Results: DNA DSBs induced by BA-mediated BNCT were primarily repaired through the homologous recombination pathway. BA-mediated BNCT induced G2/M arrest and apoptosis in HCC. Conclusion: Our findings may enable the identification of radiosensitizers or adjuvant drugs for potentiating the therapeutic effectiveness of BA-mediated BNCT for HCC.