Objective To explore the expression and clinical significance of inhibitor of DNA binding 1 (ID-1) in breast cancer and its molecular mechanism in human breast cancer MCF-7 cells by targeting the nuclear factor (NF)-κB / Src homology 2 domain-containing protein tyrosine phosphatase ( SHP2) / SMAD/ Src signaling pathway. Methods The expression of ID-1 in breast cancer tissues and adjacent normal tissues was detected using immunohistochemistry, and its clinical significance was analyzed. Bioinformatics analysis was employed to examine the correlation between ID-1 and key proteins. In the in vivo experiment, 45 female mice were selected to establish a breast cancer model and divided into five groups with 9 mice each: Vivo-control group, Vivo-BMP2 group, Vivo-ID-1 mimic + BMP2 group, Vivo-BMP2 + PHPS1 group, and Vivo-ID-1 mimic + PHPS1 group. Tumor tissues from each group were dissected, observed, and weighed. Human breast cancer MCF-7 cells were used for in vitro experiments and divided into NC group, BMP2 group, ID-1 mimic+BMP2 group, sulfasalazine+BMP2 group, ID-1 mimic+sulfasalazine+BMP2 group, BMP2+PHPS1 group, and ID-1 mimic+BMP2+PHPS1 group. Protein expression levels were determined by Western blot, and cell migration and cell invasion were evaluated by scratch and Transwell assays, respectively. Results Immunohistochemical result showed that the expression of ID-1 in breast cancer tissues was significantly higher than that in adjacent normal tissues, the difference was statistically significant (P<0. 001). The expression status of ID-1 was closely associated with histological grade, TNM stage, lymph node metastasis, and distant metastasis ( P<0. 05). Bioinformatics analysis indicated that ID-1 was correlated with BMP2, NF-κB,SMAD1 / 8, and Src in breast cancer(P<0. 05). ID-1 promoted the progression of breast cancer tumors in vivo, while inhibition of SHP2 slowed tumor progression ( P<0. 05, P<0. 01). Inhibition of SHP2 significantly decreased expression levels of ID-1, NF-κB, phospho ( p)-SHP2, p-SMAD1 / 5 / 8, and p-Src proteins in vitro( P<0. 05,P<0. 01). Similarly, inhibition of NF-κB reduced expression levels of ID-1, NF-κB, p-SHP2, p-SMAD1 / 5 / 8, and pSrc proteins(P<0. 05,P<0. 01). Both ID-1 and BMP2 promoted MCF-7 cell migration, while inhibition of SHP2 or NF-κB significantly reduced cell migration(P<0. 05,P<0. 01). ID-1 and BMP2 also enhanced MCF-7 cell invasion,while inhibition of SHP2 or NF-κB reduced cell invasion( P<0. 05,P<0. 01). Conclusions ID-1 may promote breast cancer invasion and migration by activating the NF-κB/ SHP2 / SMAD/ Src signaling pathway.