Abstract: Objective: To explore the effects of sulforaphane (SFN) on the proliferation, cycle, metastasis, and apoptosis of pancreatic cancer PANC-1 cells and its mechanism. Methods: PANC-1 cells were randomly divided into four groups: control (sh-NC), SFN (sh-NC+SFN), experimental (sh-TP53), and sh-TP53+SFN. Various SFN concentrations (0, 6, 8, 10, 16 and 20 μg/mL) were prepared. The cell survival rate was assessed using a cell counting kit-8 (CCK-8), scratch and Transwell assays were conducted to assess migration and invasion abilities of the cell, while flow cytometry was utilized to analyze the cell cycle and apoptosis capacity. The expression levels of apoptotic proteins B-cell lymphoma 2 associated X protein (Bax), B-cell lymphoma 2 (Bcl-2) , cysteinyl aspartate specific proteinase-3 (Caspase-3) and cysteinyl aspartate specific proteinase-9 (Caspase-9), cell cycle proteins cyclin-dependent protein kinase 1 (CDK1) and cyclin B, matrix metallopeptidase-9 (MMP-9) and E-cadherin, and p53 signaling pathway growth arrest and DNA damage inducible alpha (GADD45A), cyclin-dependent kinase inhibitors 1A (p21) and tumor protein p53 (TP53) gene were detected using western blotting (WB), which were used to observe its effects on SFN regulated cell proliferation and p53 signaling pathway. Results: SFN reduced PANC-1 cell proliferation in a concentration-dependent manner. In contrast to the control group, the proliferation rate of PANC-1 cells treated with SFN was significantly decreased (P<0.001). Migration and invasion abilities were weakened (P<0.01, P<0.0001). Arrested PANC-1 cells in the G2/M phase (P<0.0001). Meanwhile, significantly promoted apoptosis (P<0.0001), and up-regulated the protein levels of Bax, Caspase-3, Caspase-9, E-cadherin, GADD45A, p21 and TP53 protein levels, down-regulated Bcl-2, CDK1, Cyclin B and MMP-9 protein levels (P<0.05, P<0.01, P<0.001, P<0.0001). In contrast to the SFN group, TP53 knockdown could significantly down-regulated the ability of SFN to inhibit PANC-1 cell proliferation, migration, invasion, and arrest in G2/M phase, significantly down-regulated the ability of SFN to promote apoptosis in PANC-1 cells, down-regulated the protein levels of Bax, Caspase-3, Caspase-9, E-cadherin, GADD45A, p21 and TP53, up-regulated the protein levels of protein levels of Bcl-2, CDK1, Cyclin B and MMP-9 (P<0.05, P<0.01, P<0.001, P<0.0001). Conclusion: SFN inhibits PANC-1 pancreatic cancer cell activity by activating the p53 signaling pathway.