李宇婷，张 雪，范 芳，李大玉，余春波，陈佳瑜，刘 云，李长福

    (1.遵义医学院 生物化学教研室，贵州 遵义 563099；2.遵义医学院 医学与生物学研究中心，贵州 遵义 563099)

    Hepatocellular carcinoma (HCC) is a common malignant solid tumor and leads the 2nd cancer mortality amongst all malignancies of the world[1].Chemotherapy is a common choice for managing patients with or without surgery.However,multidrug resistance (MDR) is almost unavoidable,and almost every HCC case shows disease progression after chemotherapy[2].The mechanisms correlated with the development of drug resistance are complicated,and one of them is DNA damage repair[3],related to the drug resistance of hepatocarcinoma cell line BEL-7402/5-FU cells as reported in previous studies[4].Commonly,DNA damage stress response prompts histone modification near the site of DNA damage,especially histone H2AX phosphorylated to γ-H2AX[5].Thus,γ-H2AX was detected as an indicator of DNA damage in this research with Mitomycin (MMC).

    Recently,Artemis,a nuclease with specific structure that participates in the non-homologous end joining (NHEJ) repair of DSBs[6],was approved that its phosphorylation by DNA-dependent protein kinase catalytic subunit (DNA-PKcs) was involved in DNA damage repair of BEL-7402/5-FU cells[7].Ataxia-Telangiectasia Mutated Protein (ATM),a protein kinase,has been shown to maintain the functional integrity of cells under DNA damage stress situation[8].However,far too little attention has been paid to whether Artemis is involved in multidrug resistance of BEL-7402/5-FU cells and whether this effect is associated with ATM. ......