BaP可诱发细胞产生多种DNA损伤应激反应(DNA damage response, DDR)。已知抑癌基因p53参与了BaP诱导的DDR。p73是p53家族成员，其异常表达也与BaP的暴露有密切联系。p73功能相互制约的两类异构体TAp73和DNp73的表达变化在肿瘤的发生于发展中发挥了关键作用，但其在DDR中的作用机制还不明确，且与已知DDR中关键因子的相互关系也有待阐明。因此，本研究分别以p53正常的L-02细胞和p53缺失的Hep3B细胞为靶细胞，建立BaP致DNA损伤的实验模型，通过siRNA、免疫荧光和流式细胞术等一系列细胞分子生物学技术，对比性研究在不同遗传背景下TAp73和DNp73对BaP诱发的DDR的影响，以及与已知DDR相关信号通路的交互作用。根据以上研究明确p73介导的p53非依赖性信号通路在BaP致DDR中的调控机理，为在分子水平阐明BaP的致癌机制提供科学依据。

BaP can induce various DNA damage response (DDR) in cells. It has been known that tumor suppressor gene p53 is involved in BaP-induced DDR. p73 is a p53 family member, its expression associates to BaP exposure. p73 has two types of isoforms TAp73 and DNp73 that perform opposite functions, and the expression levels of the two isoforms play important roles in cancer development. However, the mechanism of TAp73 and DNp73 in BaP-induced DDR is unclear, and the interactions of TAp73/DNp73 with key factors of DDR remain to be elucidated. This study takes p53-proficient L-02 and p53-deficient Hep3B cells as targets, establish BaP-induced DNA damage cell models, using a series of cellular and molecular techniques such as siRNA, immunofluorescence and flow cytometry, under different genetic background, to analyze the effect of TAp73/DNp73 on BaP-induced DDR, and the interactions of TAp73/DNp73 with key factors of DDR, to clarify the regulation of p73-mediated and p53 independent cell signaling in BaP-induced DDR, and to supply evidence to elucidate the oncogenic mechanism of BaP at molecular level.