Objective: To explore the expression and clinical significance of ID-1 in breast cancer and the molecular mechanism of regulating the progression of human breast cancer MCF-7 cells by targeting NF-κB/SHP2/SMAD/Src signaling pathway; Methods: Immunohistochemistry was used to detect the expression of ID-1 in breast cancer tissues and adjacent normal tissues, and its clinical significance was analyzed. The correlation between ID-1 and key proteins was analyzed by bioinformatics. In an in vivo experiment, 45 female mice were used to establish a breast cancer model and were divided into 5 groups: NC group (Group 1), BMP2 group (Group 2), ID-1 mimic+BMP2 group (Group 3), BMP2+PHPS1 group (Group 4), and ID-1 mimic+PHPS1 group (Group 5). Tumor tissues from the five groups of mice were dissected, observed, and weighed. In an in vitro experiment, Human breast cancer MCF-7 cells were divided into 7 groups: NC group (Group 1), BMP2 group (Group 2), ID-1 mimic+BMP2 group (Group 3), sulfasalazine+BMP2 group (Group 4), ID-1 mimic+sulfasalazine+BMP2 group (Group 5), BMP2+PHPS1 group (Group 6), and ID-1 mimic+BMP2+PHPS1 group (Group 7). Western blot analysis was conducted to assess protein expression in the various groups. Scratch assays were used to evaluate MCF-7 cell migration, while Transwell assays were employed to assess MCF-7 cell invasion; Results: Immunohistochemical results showed that the expression of ID-1 in breast cancer tissues was significantly higher than that in adjacent normal tissues, mainly in the nucleus and cytoplasm, and the difference was statistically significant (P<0.001). The expression status of ID-1 was closely related to histological grade, TNM stage, lymph node metastasis and distant metastasis, and the differences were statistically significant, P<0.05; Bioinformatics correlation analysis indicated that ID-1 was correlated with BMP2, NF-κB, SHP2, SMAD and Src in breast cancer. The results of in vivo experiments showed that ID-1 was proved to promote the progression of breast cancer tumors, while inhibition of SHP2 slowed down tumor progression. The results of in vitro experiments showed that inhibition of SHP2 led to significant decreases in the expression of ID-1, NFκB, P-SHP2, P-SMAD1/5/8, and P-Src proteins. Similarly, inhibition of NF-κB resulted in reduced expression of ID-1, NF-κB, P-SHP2, P-SMAD1/5/8, and P-Src proteins. Scratch assays demonstrated that both ID-1 and BMP2 promoted MCF-7 cell migration, while inhibition of SHP2 or NF-κB significantly reduced cell migration. Transwell assays revealed that ID-1 and BMP2 enhanced MCF-7 cell invasion, with inhibition of SHP2 or NFκB leading to a marked reduction in cell invasion. Conclusion: ID-1 may promote breast cancer invasion and migration by activating the NFκB/SHP2/SMAD/Src signaling pathway.