In the current study, the expression of PARP1 in the blood samples showed a high consistency with that in the tissue samples, which indicated that the expression of PARP1 in blood could instruct the expression in tissue. Because of that, the related information about the development of tumor could be obtained through the detection of PARP1 expression in blood at the early stage of NSCLC tumor. The results of MTT assays indicated that lockdown of PARP1 gene significantly inhibited the cell growth of A549, H1975 and PC9, while PARP1 overexpression promoted the growth of A431 cell significantly. It indicated that PARP1 gene promoted the proliferation of NSCLC, whose role was consistent in others malignant tumor [27, 28]. There were many extensive researches on the gene which influence NSCLC cell migration, mainly including MALAT-1 , MTA1 , BRAF , EGFR and so on. However, the role of PARP1 in NSCLC migration remains still unknown. Our experiments revealed that: expression of PARP1 was upregulated in NSCLC and showed higher expression in metastatic NSCLC; PARP1 silence inhibited cell migration significantly, while PARP1 overexpression promoted NSCLC cell migration significantly . It has demonstrated that knockout or inhibition of PARP1 could decrease the migration of lung adenocarcinoma significantly, which indicated PARP1 was involved in the migration of NSCLC. In addition, there was a direct association between PARP1 and the key cancer gene of NSCLC: EGFR, ALK in the interaction network of genes. Previous studies have suggested that EGFR takes part in DNA repair through PI3K signaling pathway [32–33]. In the cells with ALK fusion, it has illustrated that dimers can be activated abnormally by aberrant receptors, which can activate the downstream signaling pathway PI3K-AKT and drive aberrant proliferation of tumor cells [34–35]. Based on these findings, it can be see that ALK and EGFR after requiring functional mutation could drive the growth of tumor cells via PI3K-AKT pathway. So we hypothesized that the effects of PARP1 on NSCLC tumor migration may be associated with the PI3K-AKT pathway. However, the mechanism needs further exploration.