Almost all the NSCLC patients would recurred in different stages, and finally suffered from disease metastasis and death . Even though there was a new development of immunotherapy and targeted therapy of tumors, once the systematic metastasis of cancer cell occurred, the five-year survival rate would decrease at lessby 10% . For that it was still a challenge to expand the survival rate of NSCLC patients by inhibiting the cell migration of cancer cells. Therefore, it was of significance for the study of molecular markers and potential therapeutic small molecules in clinical stage. PARP1 played an important role in DNA damage repair, especially in base excision repair (BER) pathway . It was further verified that PARP1 played a key role in DNA repair [15–17], which made PARP1 a valuable therapeutic target in the research of disease drug. Recently, it was found that PARP1 presented high expression in a series of cancers, which provided a high-value target for the study of tumor detection, stage and biological characteristics [18–23]. The overexpression of PARP1 results from much DNA damage in cancer cells with unstable genes, instead of the induction of the activated specific carcinogenic pathway . Byers, et al. demonstrated that PARP1 could be a new target molecule for NSCLC by combined transcriptome and proteome analysis . Meanwhile, a new study claimed that PARP1 could promote the metastasis and recurrence of lung adenocarcinoma towards brain and bones by regulating several steps in the metastasis process, which was not related to DNA repair. There were several ways of PARP1 enhancing the metastasis of lung adenocarcinoma towards brain: promoting the invasion of lung adenocarcinoma cells, anoikis resistance, exosmosis, and self-updating, as well as regulating cerebral microenvironment .